organic, nano-scale, biologically-integrated, self assembling electronics are here, functioning, and now inside of you and I

Organic, nano-scale, biologically-integrated, self-assembling semi-conductor electronics are here, functioning, and now inside of you and I

You have allready been exposed and you simply do not yet realise it.



My name is TIMOTHYTRESPAS and my wife, PETRA SCHILLER and I have discovered we are TARGETED INDIVIDUALS.

AS such we have been exposed to the latest military technology and human experimentation under REMOTE NEURAL MONITORING, synthetic telepathy, GENETIC MANIPULATION through exposure to such organisms as MORGELLONS a weaponized GMO designed to infect human beings, self asemble the required organic nano-electronincs via cellular, chemical, genetic, and biological processees, and allow the target to be ‘connected’ to the ‘network’ of monitoring torture and control.

Here is some information to give direction to those thinkers who desire to discover the possible basis for these covert technologies, being deloyed on a global scale as you read this.

You have allready been exposed and you simply do not yet realise it.



This all started by a thought about how we had some ‘things’ shooting out of the top of our heads every 12 or so min. they would shoot up in the air and grow larger as they flew/fell reaching about 1-2 inches at the most.

When they reached the ground they would instantly change color in a pattern that would match whatever it was on. rock, grass, ground. Like an animal that changes color to match its surroundings.

(I had recorded it on video only to find the next day my phone had had the card removed and water had been dripped inside of my new 200$ phone. The evidence was gone, along with much other video of people with gas masks on sneaking around our hotel and horrible insects emerging from or skin ad who knows what else was destroyed by these shifters with a desire to remain covert)

I was positing a theory that part of what we were exposed to was a genetic manipulation. an organism that was able to transfer genes across lines, cells that migrate those genes, genetic information or code segments to ‘create’ the creatures (there were man ‘bugs’ and other ‘creatures’ that seemed to emerge from inside of us, also living creatures that seemed to be made of materials other than normal, such as metals or other unknown ‘electronic’ looking materials) and the gene segments required for the process of ‘biogenesis’ or the creation of full grown creatures from inside of a living organism assembled from gene segments via a process this exploration is attempting to shed light on.

record everything

record everything

I am not a geneticists, nor a microbiologist, nor a nano-materials engineer, nor man of the disciplines required to create such a ‘system’.

But I am smart enough (for the moment, GOD wiling) to possibly understand the concept of what may have been done.

each time we investigate a new bit of the puzzle may become known and one day (GOD willing) the entire picture will be known, shown, and taken responsibility for.

Please, if your brain can stand it, take some time to read over these concepts.

I think you will find some answers here regarding what may have been done to you/me/us.

It is a complicated operation with many facets.

genetics is only one.

  • electromagnetics,
  • biophotonics,
  • scalar energy,
  • information transfer,
  • microwave energy,
  • interferometry,
  • metamaterials science,
  • nanotechnology,
  • micro-fluidics,
  • micro-magnetics,
  • self assembling materials,
  • chimeras,
  • in-vivo gene segmentation and re-transcription,
  • and GOD only knows how many other disciplines involved to create the package that is the modern day mind control remote neural monitoring tracking,
  • no touch torture,
  • monitoring thoughts, speech, eyesight, hearing, dreams, bio-data,
  • and allowing a two way 24//365 open pathway into your subconscious mind (allowing for hypnotic induction and manipulation of all thoughts and emotions) and
  • direct access to the conscious mind as well via synthetic telepathy and
  • superluminal scalar bio-telemetric/neuro-telemetric data systems

all installed into the human population through an organism designed to do just that: MORGELLONS


and get this finding: use of chromophore-based circuitry will/has create/created nano-sized electronic components .

organic, nano-scale, biologically-integrated, self assembling electronics are here, functioning, and now inside of you and I.

Global mind control, genetics control,cloning, neural mapping, artificial intelligence, microwave no-touch torture, induced sickness, monitoring of all thoughts, dreams speach, sight, actions, sounds, etc.

and you thought “BIG BROTHER’ was just a silly idea in a book…

Read some of this science and see the possibilities come true…


The enteric nervous system (ENS) or intrinsic nervous system is one of the main divisions of the autonomic nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system.[1]

It is derived from neural crest.

The enteric nervous system consists of some one hundred million neurons,[4] one thousandth of the number of neurons in the brain, and essentially equal to the one hundred million neurons in the spinal cord. [5] The enteric nervous system is embedded in the lining of the gastrointestinal system, beginning in the esophagus and extending down to the anus. [6]

The neurons of the ENS are collected into two types of ganglia: myenteric (Auerbach’s) and submucosal (Meissner’s) plexuses.[7] Myenteric plexuses are located between the inner and outer layers of the muscularis externa, while submucosal plexuses are located in the submucosa.


The ENS is capable of autonomous functions[8] such as the coordination of reflexes; although it receives considerable innervation from the autonomic nervous system, it can and does operate independently of the brain and the spinal cord.[9] Its study is the focus of neurogastroenterology.

ENS function can be damaged by ischemia.[10] Transplantation, which had been described as a theoretical possibility,[11] is now (As of 2011) a clinical reality in the United States and is performed at a number of approved centers.[12]


The enteric nervous system has been described as a “second brain” for several reasons.

The enteric nervous system can operate autonomously. It normally communicates with the central nervous system (CNS) through the parasympathetic (e.g., via the vagus nerve) and sympathetic (e.g., via the prevertebral ganglia) nervous systems. However, vertebrate studies show that when the vagus nerve is severed, the enteric nervous system continues to function.[13]

In vertebrates the enteric nervous system includes efferent neurons, afferent neurons, and interneurons, all of which make the enteric nervous system capable of carrying reflexes and acting as an integrating center in the absence of CNS input. The sensory neurons report on mechanical and chemical conditions. Through intestinal muscles, the motor neurons control peristalsis and churning of intestinal contents. Other neurons control the secretion of enzymes. The enteric nervous system also makes use of more than 30 neurotransmitters, most of which are identical to the ones found in CNS, such as acetylcholine, dopamine, and serotonin. More than 90% of the body’s serotonin lies in the gut, as well as about 50% of the body’s dopamine, which is currently being studied to further our understanding of its utility in the brain.


Neural crest cells are a transient, multipotent, migratory cell population unique to vertebrates that gives rise to a diverse cell lineage including melanocytes, craniofacial cartilage and bone, smooth muscle, peripheral and enteric neurons and glia.[1]

After gastrulation, neural crest cells are specified at the border of the neural plate and the non-neural ectoderm. During neurulation, the borders of the neural plate, also known as the neural folds, converge at the dorsal midline to form the neural tube. Subsequently, neural crest cells from the roof plate of the neural tube undergo an epithelial to mesenchymal transition, delaminating from the neuroepithelium and migrating through the periphery where they differentiate into varied cell types.[1] The emergence of neural crest was important in vertebrate evolution because many of its structural derivatives are defining features of the vertebrate clade.[2]

Underlying the development of neural crest is a gene regulatory network, described as a set of interacting signals. transcription factors, and downstream effector genes that confer cell characteristics such as multipotency and migratory capabilities.[3]

Understanding the molecular mechanisms of neural crest formation is important for our knowledge of human disease because of its contributions to multiple cell lineages. Abnormalities in neural crest development cause neurocristopathies, which include conditions such frontonasal dysplasiasa, Waardenburg-Shah syndrome, and DiGeorge syndrome.[1]

Therefore, defining the mechanisms of neural crest development may reveal key insights into vertebrate evolution and neurocristopathies.


Chimeras, generated through transplantation, enabled researchers to distinguish neural crest cells of one species from the surrounding tissue of another species. With this technique, generations of scientists were able to reliably mark and study the ontogeny of neural crest cells.

Neural Crest.

Putative neural crest gene-regulatory network functioning at the neural plate border in vertebrates. Red arrows represent proven direct regulatory interactions. Black arrows show genetic interactions based on loss-of-function and gain-of-functions studies. Gray lines denote repression. Adapted from Bronner-Fraser 2004.


A molecular cascade of events is involved in establishing the migratory and multipotent characteristics of neural crest cells. This gene-regulatory network can be subdivided into the following four sub-networks described below.

Inductive signals

First, extracellular signaling molecules, secreted from the adjacent epidermis and underlying mesoderm such Wnts, BMPs and Fgfs separate the non-neural ectoderm (epidermis) from the neural plate during neural induction.[1][2]

Wnt signaling has been demonstrated in neural crest induction in several species through gain-of-function and loss-of-function experiments. In coherence with this observation, the promoter region of slug (a neural crest specific gene) contains a binding site for transcription factors involved in the activation of Wnt-dependent target genes, suggestive of a direct role of Wnt signaling in neural crest specification.[8]

The current role of BMP in neural crest formation is associated with the induction of the neural plate. BMP antagonists diffusing from the ectoderm generates a gradient of BMP activity. In this manner, the neural crest lineage forms from intermediate levels of BMP signaling required for the development of the neural plate (low BMP) and epidermis (high BMP).[1]

Fgf from the paraxial mesoderm has been suggested as a source of neural crest inductive signal. Researchers have demonstrated that the expression of dominate-negative Fgf receptor in ectoderm explants blocks neural crest induction when recombined with paraxial mesoderm.[9] Our current understanding of the role of BMP, Wnt, and Fgf pathways on neural crest specifier expression remains incomplete.

Neural plate border specifiers

Signaling events that establish the neural plate border lead to the expression of a set of transcription factors delineated here as neural plate border specifiers. These molecules include Zic factors, Pax3/7, Dlx5, Msx1/2 which may mediate the influence of Wnts, BMPs, and Fgfs. These genes are expressed broadly at the neural plate border region and precede the expression of bona fide neural crest markers.[2]

Experimental evidence places these transcription factors upstream of neural crest specifiers. For example, in Xenopus Msx1 is necessary and sufficient for the expression of Slug, Snail, and FoxD3.[10] Furthermore, Pax3 is essential for FoxD3 expression in mouse embryos.[11]

Neural crest specifiers

Following the expression of neural plate border specifiers is a collection of genes including Slug/Snail, FoxD3, Sox10, Sox9, AP-2 and c-Myc. This suite of genes, designated here as neural crest specifiers, are activated in emergent neural crest cells. At least in Xenopus, every neural crest specifier is necessary and/or sufficient for the expression of all other specifiers, demonstrating the existence of extensive cross-regulation.[2]

Outside of the tightly regulated network of neural crest specifiers are two other transcription factors Twist and Id. Twist, a bHLH transcription factor, is required for mesenchyme differentiation of the pharyngeal arch structures.[12] Id is a direct target of c-Myc and is known to be important for the maintenance of neural crest stem cells.[13]

Neural crest effector genes

Finally, neural crest specifiers turn on the expression of effector genes, which confer certain properties such as migration and multipotency. Two neural crest effectors, Rho GTPases and cadherins, function in delamination by regulating cell morphology and adhesive properties. Sox9 and Sox10 regulate neural crest differentiation by activating many cell-type-specific effectors including Mitf, P0, Cx32, Trp and cKit.[2]

Cell lineages

Neural crest cells originating from different positions along the anterior-posterior axis develop into various tissues. These regions of neural crest can be divided into four main functional domains, which include the cranial neural crest, trunk neural crest, vagal and sacral neural crest, and cardiac neural crest.

Cranial neural crest

Cranial neural crest migrates dorsolaterally to form the craniofacial mesenchyme that differentiates into various cranial ganglia and craniofacial cartilages and bones.[14] These cells enter the pharyngeal pouches and arches where they contribute to the thymus, bones of the middle ear and jaw and the odontoblasts of the tooth primordia.[15]

Trunk neural crest

Trunk neural crest gives rise to two populations of cells. One group of cells fated to become melanocytes migrates dorsolaterally into the ectoderm towards the ventral midline. A second group of cells migrates ventrolaterally through the anterior portion of each sclerotome. The cells that stay in the sclerotome form the dorsal root ganglia, whereas those that continue more ventrally form the sympathetic ganglia, adrenal medulla, and the nerves surrounding the aorta.[15]

Vagal and sacral neural crest

The vagal and sacral neural crest cells develop into the ganglia of the enteric nervous system and the parasympathetic ganglia.[15]

Cardiac neural crest

Cardiac neural crest develops into melanocytes, cartilage, connective tissue and neurons of some pharyngeal arches. Also, this domain gives rise to regions of the heart such as the musculo-connective tissue of the large arteries, and part of the septum, which divides the pulmonary circulation from the aorta.[15] The semilunar valves of the heart are associated with neural crest cells according to new research.[16]


Several structures that distinguish the vertebrates from other chordates are formed from the derivatives of neural crest cells. In their “New head” theory, Gans and Northcut argue that the presence of neural crest was the basis for vertebrate specific features, such as sensory ganglia and cranial skeleton. Furthermore, the appearance of these features was pivotal in vertebrate evolution because it enabled a predatory lifestyle.[17]

However, considering the neural crest a vertebrate innovation does not mean that it was created de novo. Instead, new structures often arise through modification of existing developmental regulatory programs. For example, regulatory programs may be changed by the co-option of new upstream regulators or by the employment of new downstream gene targets, thus placing existing networks in a novel context.[18][19] This idea is supported by in situ hybridization data that shows the conservation of the neural plate border specifiers in protochordates, which suggest that part of the neural crest precursor network was present in a common ancestor to the chordates.[3] In some non-vertebrate chordates such as tunicates a lineage of cells (melanocytes) has been identified, which are similar to neural crest cells in vertebrates. This implies that a rudimentary neural crest existed in a common ancestor of vertebrates and tunicates.[20]

Neural Crest derivatives

Mesectoderm:[21] odontoblasts, dental papillae, the chondrocranium (nasal capsule, Meckel’s cartilage, scleral ossicles, quadrate, articular, hyoid and columella), tracheal and laryngeal cartilage, the dermatocranium (membranous bones), dorsal fins and the turtle plastron (lower vertebrates), pericytes and smooth muscle of branchial arteries and veins, tendons of ocular and masticatory muscles, connective tissue of head and neck glands (pituitary, salivary, lachrymal, thymus, thyroid) dermis and adipose tissue of calvaria, ventral neck and face

Endocrine Cells: chromaffin cells of the adrenal medulla, parafollicular cells of the thyroid, glomus cells type I/II

Peripheral nervous system: Sensory neurons and glia of the dorsal root ganglia, cephalic ganglia (VII and in part, V, IX, and X), Rohon-Beard cells, some Merkel cells in the whisker,[22][23] Satellite glial cells of all autonomic and sensory ganglia, Schwann cells of all peripheral nerves

Melanocytes and iris pigment cells

See also


A chimera (also spelled chimaera) is a single organism composed of genetically distinct cells. This can result in male and female organs, two different blood types, or subtle variations in form.[1] Animal chimeras are produced by the merger of multiple fertilized eggs. In plant chimeras, however, the distinct types of tissue may originate from the same zygote, and the difference is often due to mutation during ordinary cell division. Normally, chimerism is not visible on casual inspection; however, it has been detected in the course of proving parentage.

Another way that chimerism can occur in animals is by organ transplantation, giving one individual tissues that developed from two different genomes. For example, a bone marrow transplant can change someone’s blood type.

An animal chimera is a single organism that is composed of two or more different populations of genetically distinct cells that originated from different zygotes involved in sexual reproduction. If the different cells have emerged from the same zygote, the organism is called a mosaic. Chimeras are formed from at least four parent cells (two fertilized eggs or early embryos fused together). Each population of cells keeps its own character and the resulting organism is a mixture of tissues. There are some reports of human chimerism.[1]

This condition is either inherited or it is acquired through the infusion of allogeneic hematopoietic cells during transplantation or transfusion. In nonidentical twins, chimerism occurs by means of blood-vessel anastomoses. The likelihood of offspring being a chimera is increased if it is created via in vitro fertilization[citation needed]. Chimeras can often breed, but the fertility and type of offspring depends on which cell line gave rise to the ovaries or testes; varying degrees of intersexuality may result if one set of cells is genetically female and another genetically male.

Tetragametic chimerism

Tetragametic chimerism is a form of congenital chimerism. This condition occurs through the fertilization of two separate ova by two sperm, followed by the fusion of the two at the blastocyst or zygote stages. This results in the development of an organism with intermingled cell lines. Put another way, the chimera is formed from the merging of two nonidentical twins (although a similar merging presumably occurs with identical twins, but as their DNA is almost identical, the presence would not be immediately detectable in a very early (zygote or blastocyst) phase). As such, they can be male, female, or hermaphroditic.

As the organism develops, it can come to possess organs that have different sets of chromosomes. For example, the chimera may have a liver composed of cells with one set of chromosomes and have a kidney composed of cells with a second set of chromosomes. This has occurred in humans, and at one time was thought to be extremely rare, though more recent evidence suggests that it is not as rare as previously believed.[1][2]

This is particularly true for the marmoset. Recent research shows most marmosets are chimeras, sharing DNA with their fraternal twins.[3] 95% of Marmoset fraternal twins trade blood through chorionic fusions, making them hematopoietic chimeras.[4][5]

Most chimeras will go through life without realizing they are chimeras. The difference in phenotypes may be subtle (e.g., having a hitchhiker’s thumb and a straight thumb, eyes of slightly different colors, differential hair growth on opposite sides of the body, etc.) or completely undetectable. Chimeras may also show, under a certain spectrum of UV light, distinctive marks on the back resembling that of arrow points pointing downwards from the shoulders down to the lower back; this is one expression of pigment unevenness called Blaschko’s lines.[6]

Affected persons may be identified by the finding of two populations of red cells or, if the zygotes are of opposite sex, ambiguous genitalia and hermaphroditism alone or in combination; such persons sometimes also have patchy skin, hair, or eye pigmentation (heterochromia). If the blastocysts are of opposite sex, genitals of both sexes may be formed, either ovary and testis, or combined ovotestes, in one rare form of intersexuality, a condition previously known as true hermaphroditism.

Note that the frequency of this condition does not indicate the true prevalence of chimerism. Most chimeras composed of both male and female cells probably do not have an intersex condition, as might be expected if the two cell populations were evenly blended throughout the body. Often, most or all of the cells of a single cell type will be composed of a single cell line, i.e. the blood may be composed prominently of one cell line, and the internal organs of the other cell line. Genitalia produce the hormones responsible for other sex characteristics. If the sex organs are homogeneous, the individual will not be expected to exhibit any intersex traits.

Natural chimeras are almost never detected unless they exhibit abnormalities such as male/female or hermaphrodite characteristics or uneven skin pigmentation. The most noticeable are some male tortoiseshell cats or animals with ambiguous sex organs.

The existence of chimerism is problematic for DNA testing, a fact with implications for family and criminal law. The Lydia Fairchild case, for example, was brought to court after DNA testing apparently showed that her children could not be hers. Fraud charges were filed against her and her custody of her children was challenged. The charge against her was dismissed when it became clear that Lydia was a chimera, with the matching DNA being found in her cervical tissue. Another case was that of Karen Keegan, who was also suspected (initially) of not being her children’s biological mother, after DNA tests on her adult sons for a kidney transplant she needed seemed to show she wasn’t their mother.[1][7]

The tetragametic state has important implications for organ or stem-cell transplantation. Chimeras typically have immunologic tolerance to both cell lines.


Microchimerism is the presence of a small number of cells that are genetically distinct from those of the host individual. Most people are born with a few cells genetically identical to their mothers’ and the proportion of these cells goes down in healthy individuals as they get older. People who retain higher numbers of cells genetically identical to their mothers’ have been observed to have higher rates of some autoimmune diseases, presumably because the immune system is responsible for destroying these cells and a common immune defect prevents it from doing so and also causes autoimmune problems. Women often also have a few cells genetically identical to that of their children, and some people also have some cells genetically identical to that of their siblings (maternal siblings only, since these cells are passed to them because their mother retained them).

Parasitic chimerism in anglerfish

Chimerism occurs naturally in adult Ceratioid anglerfish and is in fact a natural and essential part of their life cycle. Once a male is born, it begins its search for a female. Using strong olfactory receptors, the male searches until it locates a female anglerfish. The male, less than an inch in length, bites into her skin and releases an enzyme that digests the skin of his mouth and her body, fusing the pair down to the blood-vessel level. While this attachment has become necessary for the male’s survival, it will eventually consume him, as both anglerfish fuse into a single hermaphroditic individual. Sometimes in this odd ritual, more than one male will attach to a single female as a ‘parasite’. They will all be consumed into the body of the larger female angler. Once fused to a female, the males will reach sexual maturity, developing large testicles as their other organs atrophy. This process allows for sperm to be in constant supply when the female produces an egg, so that the chimeric fish is able to have a greater number of offspring.[8]

Germline chimerism

Germline chimerism occurs when the germ cells (for example, sperm and egg cells) of an organism are not genetically identical to its own. It has recently been discovered that marmosets can carry the reproductive cells of their (fraternal) twin siblings, because of placental fusion during development. (Marmosets almost always give birth to fraternal twins.)[3][9][10]


  • The Dutch sprinter Foekje Dillema was expelled from the 1950 national team after she refused a mandatory sex test in July 1950; later investigations revealed a Y-chromosome in her body cells, and the analysis showed that she probably was a 46,XX/46,XY mosaic female.[11]
  • In 1953 a human chimera was reported in the British Medical Journal. A woman was found to have blood containing two different blood types. Apparently this resulted from her twin brother’s cells living in her body.[12] More recently, a study found that such blood group chimerism is not rare.[13]
  • Another report of a human chimera was published in 1998, where a male human had some partially developed female organs due to chimerism. He had been conceived by in-vitro fertilization.[14]
  • In 2002, Lydia Fairchild was denied public assistance when DNA evidence showed that she was not related to her children. A lawyer for the prosecution heard of a human chimera in New England, Karen Keegan, and suggested the possibility to the defence, who were able to show that Fairchild, too, was a chimera with two sets of DNA.[15]


In biological research, chimeras are artificially produced by selectively transplanting embryonic cells from one organism onto the embryo of another, and allowing the resultant blastocyst to develop. Chimeras are not hybrids, which form from the fusion of gametes from two species that form a single zygote with a combined genetic makeup, or Hybridomas which, as with hybrids, result from fusion of two species’ cells into a single cell and artificial propagation of this cell in the laboratory. Essentially, in a chimera, each cell is from either of the parent species, whereas in a hybrid and hybridoma, each cell is derived from both parent species. “Chimera” is a broad term and is often applied to many different mechanisms of the mixing of cells from two different species.

As with cloning, the process of creating and implanting a chimera is imprecise, with the majority of embryos spontaneously terminating. Successes, however, have led to major advancements in the field of embryology, as creating chimeras of one species with different physical traits, such as colour, has allowed researchers to trace the differentiation of embryonic cells through the formation of organ systems in the adult individual.

The first known primate chimeras are the twins Roku and Hex; each having 6 genomes. They were created by mixing cells from toripotent 4 cell blastocysts; although the cells never fused they worked together to form organs. It was discovered that one of these primates Roku was a sexual chimera; as four percent of Roku’s blood cells contained two x chromosomes.[4]

A major milestone in chimera experimentation occurred in 1984, when a chimeric geep was produced by combining embryos from a goat and a sheep, and survived to adulthood.[16] The creation of the “geep” revealed several complexities to chimera development. In implanting a goat embryo for gestation in a sheep, the sheep’s immune system would reject the developing goat embryo, whereas a “geep” embryo, sharing markers of immunity with both sheep and goats, was able to survive implantation in either of its parent species.

In August 2003, researchers at the Shanghai Second Medical University in China reported that they had successfully fused human skin cells and dead rabbit eggs to create the first human chimeric embryos. The embryos were allowed to develop for several days in a laboratory setting, then destroyed to harvest the resulting stem cells.[17] In 2007, scientists at the University of Nevada School of Medicine created a sheep whose blood contained 15% human cells and 85% sheep cells.[18] The implications of increasingly realizable projects using human-animal hybrids for biopharmaceutical production, and potentially for producing cells or organs, have raised a host of ethical and safety issues.


Chimeric mice are important tools in biological research, as they allow the investigation of a variety of biological questions in an animal that has two distinct genetic pools within it. These include insights into such problems as the tissue specific requirements of a gene, cell lineage, and cell potential. The general methods for creating chimeric mice can be summarized either by injection or aggregation of embryonic cells from different origins. The first chimeric mouse was made by Beatrice Mintz in the 1960s through the aggregation of eight cell stage embryos.[19] Injection on the other hand was pioneered by Richard Gardner and Ralph Brinster who injected cells into blastocysts to create chimeric mice with germ lines fully derived from injected ES Cells.[20] Chimeras can be derived from mouse embryos that have not yet implanted in the uterus as well as from implanted embryos. ES cells from the inner cell mass of an implanted blastocyst can contribute to all cell lineages of a mouse including the germ line. ES cells are also a useful tool in chimeras because genes can be mutated in them through the use of homologous recombination, thus allowing gene targeting. Since this discovery occurred in 1999, ES cells have become a key tool in the generation of specific chimeric mice.[21]

Underlying biology

The ability to make mouse chimeras comes from an understanding of early mouse development. Between the stages of fertilization of the egg and the implantation of a blastocyst into the uterus, different parts of the mouse embryo retain the ability to give rise to a variety of cell lineages. Once the embryo has reached the blastocyst stage, it is composed of several parts, mainly the trophectoderm, the inner cell mass, and the primitive endoderm. Each of these parts of the blastocyst gives rise to different parts of the embryo; the inner cell mass gives rise to the embryo proper, while the trophectoderm and primitive endoderm give rise to extra embryonic structures that support growth of the embryo.[22] Two- to eight-cell-stage embryos are competent for making chimeras, since at these stages of development, the cells in the embryos are not yet committed to give rise to any particular cell lineage, and could give rise to the inner cell mass or the trophectoderm. In the case where two diploid eight-cell-stage embryos are used to make a chimera, chimerism can be later found in the epiblast, primitive, endoderm and trophectoderm of the mouse blastocyst.[23][24] It is possible to dissect the embryo at other stages so as to accordingly give rise to one lineage of cells from an embryo selectively and not the other. For example, subsets of blastomeres can be used to give rise to chimera with specified cell lineage from one embryo. The Inner Cell Mass of a diploid blastocyst for example can be used to make a chimera with another blastocyst of eight-cell diploid embryo; the cells taken from the inner cell mass will give rise to the primitive endoderm and to the epiblast in the chimera mouse.[25] From this knowledge, ES cell contributions to chimeras have been developed. ES cells can be used in combination with eight-cell-and two-cell-stage embryos to make chimeras and exclusively give rise to the embryo proper. Embryos that are to be used in chimeras can further be genetically altered in order to specifically contribute to only one part of chimera. An example is the chimera built off of ES cells and tetraploid embryos, tetraploid embryos which are artificially made by electrofusion of two two-cell diploid embryos. The tetraploid embryo will exclusively give rise to the trophectoderm and primitive endoderm in the chimera[26][27]

Methods of production

There are a variety of combinations that can give rise to a successful chimera mouse and — according to the goal of the experiment — an appropriate cell and embryo combination can be picked; they are generally but not limited to diploid embryo and ES cells, diploid embryo and diploid embryo, ES cell and tetraploid embryo, diploid embryo and tetraploid embryo, ES cells and ES cells. The combination of embryonic stem cell and diploid embryo is a common technique used for the making of chimeric mice, since gene targeting can be done in the embryonic stem cell. These kinds of chimeras can be made through either aggregation of stem cells and the diploid embryo or injection of the stem cells into the diploid embryo. If embryonic stem cells are to be used for gene targeting to make a chimera, the following procedure is common: a construct for homologous recombination for the gene targeted will be introduced into cultured mouse embryonic stem cells from the donor mouse, by way of electroporation; cells positive for the recombination event will have antibiotic resistance, provided by the insertion cassette used in the gene targeting; and be able to be positively selected for.[28][29] ES cells with the correct targeted gene are then injected into a diploid host mouse blastocyst. These injected blastocysts are then implanted into a pseudo pregnant female surrogate mouse which will bring the embryos to term and give birth to a mouse whose germline is derived from the donor mouse’s ES cells.[30] This same procedure can be achieved through aggregation of ES cells and diploid embryos, diploid embryos are cultured in aggregation plates in wells where single embryos can fit, to these wells ES cells are added the aggregates are cultured until a single embryo is formed and has progressed to the blastocyst stage, and can then be transferred to the surrogate mouse.[31]



The distinction between sectorial, mericlinal and periclinal chimeras are widely used.[32][33]

Graft chimeras

Taxus mosaic.

These are produced by grafting tetically different parents, different cultivars or different species (which may belong to different genera). The tissues may be partially fused together following grafting to form a single growing organism that preserves both types of tissue in a single shoot.[34] Just as the constituent species are likely to differ in a wide range of features, so the behavior of their periclinal chimeras is like to be highly variable.[35] The first such known chimera was probably the Bizzaria which is a confusion of the Florentine citron and the sour orange. Perhaps the best-known example of a graft-chimera is Laburnocytisus ‘Adamii’, caused by a fusion of a Laburnum and a broom.

Chromosomal chimeras

These are chimeras in which the layers differ in their chromosome constitution. Occasionally chimeras arise from loss or gain of individual chromosomes or chromosome fragments owing to misdivision.[36] More commonly cytochimeras have simple multiple of the normal chromosome complement in the changed layer. There are various effects on cell size and growth characteristics.

Nuclear gene-differential chimeras

These chimeras arise by spontaneous or induced mutation of a nuclear gene to a dominant or recessive allele. As a rule one character is affected at a time in the leaf, flower, fruit, or other parts.

Plastid gene-differential chimeras

These chimeras arise by spontaneous or induced mutation of a plastid gene, followed by the sorting-out of two kinds of plastid during vegetative growth. Alternatively, after selfing or nucleic acid thermodynamics, plastids may sort-out from a mixed egg or mixed zygote respectively. This type of chimera is recognized at the time of origin by the sorting-out pattern in the leaves. After sorting-out is complete, periclinal chimeras are distinguished from similar looking nuclear gene-differential chimeras by their non-mendelian inheritance. The majority of variegated-leaf chimeras are of this kind.

All plastid gene- and some nuclear gene-differential chimeras affect the color of the plasmids within the leaves, and these are grouped together as chlorophyll chimeras, or preferably as variegated leaf chimeras. For most variegation, the mutation involved is the loss of the chloroplasts in the mutated tissue, so that part of the plant tissue has no green pigment and no photosynthetic ability. This mutated tissue is unable to survive on its own but is kept alive by its partnership with normal photosynthetic tissue. Sometimes chimeras are also found with layers differing in respect of both their nuclear and their plastid genes.


There are multiple reasons to explain the occurrence of plant chimera during plant recovery stage. (1)The process of shoot organogenesis starts form the multicellular origin.[37] (2)The endogenous tolerance leads to the ineffectiveness of the weak selective agents. (3)A self-protection mechanism (cross protection). Transformed cells serve as guards to protect the untransformed ones.[38] (4)The observable characteristic of transgenic cells may be a transient expression of the marker gene. Or it may due to the presence of agrobacterium cells.


Untransformed cells should be easy to detect and remove to avoid chimeras. Because it’s extremely important to maintain the stable ability of the transgenic plants across different generations. Reporter genes such as GUS and Green Fluorescent Protein[39](GFP) are utilized in combination with plant selective markers (herbicide, antibody etc.) However, GUS expression depends on the plant development stage and GFP may be influenced by the green tissue autofluorescence. Quantitative PCR could be an alternative method for chimera detection.[40]


The US and Western Europe have strict codes of ethics and regulations in place that expressly forbid certain subsets of experimentation using human cells, though there is a vast difference in the regulatory framework.[41] In May 2008, a robust debate in the House of Commons of the United Kingdom on the ethics of creating chimeras with human stem cells led to the decision that embryos would be allowed to be made in laboratories, given that they would be destroyed within the first 14 days. No such foundation has been set for chimera research regulation in the US.


Chromatophores are pigment-containing and light-reflecting organelles in cells found in a wide range of animals including amphibians, fish, reptiles, crustaceans, cephalopods, and bacteria. Mammals and birds, in contrast, have a class of cells called melanocytes with a similar function.

Chromatophores are largely responsible for generating skin and eye colour in cold-blooded animals and are generated in the neural crest during embryonic development. Mature chromatophores are grouped into subclasses based on their colour (more properly “hue“) under white light: xanthophores (yellow), erythrophores (red), iridophores (reflective / iridescent), leucophores (white), melanophores (black/brown), and cyanophores (blue). The term can also refer to coloured, membrane-associated vesicles found in some forms of photosynthetic bacteria.

Some species can rapidly change colour through mechanisms that translocate pigment and reorient reflective plates within chromatophores. This process, often used as a type of camouflage, is called physiological colour change or metachrosis.[1] Cephalopods such as the octopus have complex chromatophore organs controlled by muscles to achieve this, whereas vertebrates such as chameleons generate a similar effect by cell signalling. Such signals can be hormones or neurotransmitters and may be initiated by changes in mood, temperature, stress or visible changes in the local environment. Chromatophores are studied by scientists to understand human disease and as a tool in drug discovery.


Aristotle mentioned the ability of the octopus to change colour for both camouflage and signalling in his Historia animalium (ca 400 BC):[2]

The octopus … seeks its prey by so changing its colour as to render it like the colour of the stones adjacent to it; it does so also when alarmed.

G. Sangiovanni was the first to describe invertebrate pigment-bearing cells as chromoforo in an Italian science journal in 1819.[3]

Charles Darwin described the colour-changing abilities of the cuttlefish in The Voyage of the Beagle (1860):[4]

These animals also escape detection by a very extraordinary, chameleon-like power of changing their colour. They appear to vary their tints according to the nature of the ground over which they pass: when in deep water, their general shade was brownish purple, but when placed on the land, or in shallow water, this dark tint changed into one of a yellowish green. The colour, examined more carefully, was a French grey, with numerous minute spots of bright yellow: the former of these varied in intensity; the latter entirely disappeared and appeared again by turns. These changes were effected in such a manner that clouds, varying in tint between a hyacinth red and a chestnut-brown, were continually passing over the body. Any part, being subjected to a slight shock of galvanism, became almost black: a similar effect, but in a less degree, was produced by scratching the skin with a needle. These clouds, or blushes as they may be called, are said to be produced by the alternate expansion and contraction of minute vesicles containing variously coloured fluids.


The term chromatophore was adopted (following Sangiovanni’s chromoforo) as the name for pigment-bearing cells derived from the neural crest of cold-blooded vertebrates and cephalopods. The word itself comes from the Greek words khrōma (χρωμα) meaning “colour,” and phoros (φορος) meaning “bearing”. In contrast, the word chromatocyte (cyte or κυτε being Greek for “cell”) was adopted for the cells responsible for colour found in birds and mammals. Only one such cell type, the melanocyte, has been identified in these animals.

It was only in the 1960s that chromatophores were well enough understood to enable them to be classified based on their appearance. This classification system persists to this day, even though the biochemistry of the pigments may be more useful to a scientific understanding of how the cells function.[5]

Colour-producing molecules fall into two distinct classes: biochromes and structural colours or “schemochromes”.[6] The biochromes include true pigments, such as carotenoids and pteridines. These pigments selectively absorb parts of the visible light spectrum that makes up white light while permitting other wavelengths to reach the eye of the observer. Structural colours are produced by various combinations of diffraction, reflection or scattering of light from structures with a scale around a quarter of the wavelength of light. Many such structures interfere with some wavelengths (colours) of light and transmit others, simply because of their scale, so they often produce iridescence, creating different colours when seen from different directions.

Whereas all chromatophores contain pigments or reflecting structures (except when there has been a mutation, as in albinism), not all pigment-containing cells are chromatophores. Haem, for example, is a biochrome responsible for the red appearance of blood. It is found primarily in red blood cells (erythrocytes), which are generated in bone marrow throughout the life of an organism, rather than being formed during embryological development. Therefore erythrocytes are not classified as chromatophores.

A veiled chameleon, Chamaeleo calyptratus. Structural green and blue colours are generated by overlaying chromatophore types to reflect filtered light.

Xanthophores and erythrophores

Chromatophores that contain large amounts of yellow pteridine pigments are named xanthophores; those with mainly red/orange carotenoids are termed erythrophores.[5] However, vesicles containing pteridine and carotenoids are sometimes found in the same cell, in which case the overall colour depends on the ratio of red and yellow pigments.[7] Therefore, the distinction between these chromatophore types is not always clear.

Most chromatophores can generate pteridines from guanosine triphosphate, but xanthophores appear to have supplemental biochemical pathways enabling them to accumulate yellow pigment. In contrast, carotenoids are metabolised and transported to erythrophores. This was first demonstrated by rearing normally green frogs on a diet of carotene-restricted crickets. The absence of carotene in the frogs’ diet meant that the red/orange carotenoid colour ‘filter’ was not present in their erythrophores. This made the frogs appear blue instead of green.[8]

Iridophores and leucophores

Iridophores, sometimes also called guanophores, are pigment cells that reflect light using plates of crystalline chemochromes made from guanine.[9] When illuminated they generate iridescent colours because of the diffraction of light within the stacked plates.

Orientation of the schemochrome determines the nature of the colour observed.[10] By using biochromes as coloured filters, iridophores create an optical effect known as Tyndall or Rayleigh scattering, producing bright-blue or –green colours.[11]

A related type of chromatophore, the leucophore, is found in some fish, in particular in the tapetum lucidum.

Like iridophores, they utilize crystalline purines (often guanine) to reflect light. Unlike iridophores, however, leucophores have more organized crystals that reduce diffraction.

Given a source of white light, they produce a white shine.

As with xanthophores and erythrophores, in fish the distinction between iridophores and leucophores is not always obvious, but, in general, iridophores are considered to generate iridescent or metallic colours, whereas leucophores produce reflective white hues.[11]


At the bottom a mutant zebrafish larva that fails to synthesise melanin in its melanophores, at the top a non-mutant, wildtype larva

Melanophores contain eumelanin, a type of melanin, that appears black or dark-brown because of its light absorbing qualities.

It is packaged in vesicles called melanosomes and distributed throughout the cell. Eumelanin is generated from tyrosine in a series of catalysed chemical reactions.

It is a complex chemical containing units of dihydroxyindole and dihydroxyindole-2-carboxylic acid with some pyrrole rings.[12]

The key enzyme in melanin synthesis is tyrosinase. When this protein is defective, no melanin can be generated resulting in certain types of albinism. In some amphibian species there are other pigments packaged alongside eumelanin. For example, a novel deep (wine) red-colour pigment was identified in the melanophores of phyllomedusine frogs.[13] This was subsequently identified as pterorhodin, a pteridine dimer that accumulates around eumelanin core, and it is also present in a variety of tree frog species from Australia and Papua New Guinea. While it is likely that other lesser-studied species have complex melanophore pigments, it is nevertheless true that the majority of melanophores studied to date do contain eumelanin exclusively.[14]

Humans have only one class of pigment cell, the mammalian equivalent of melanophores, to generate skin, hair, and eye colour. For this reason, and because the large number and contrasting colour of the cells usually make them very easy to visualise, melanophores are by far the most widely studied chromatophore. However, there are differences between the biology of melanophores and that of melanocytes. In addition to eumelanin, melanocytes can generate a yellow/red pigment called phaeomelanin.

The purple-striped dottyback, Pseudochromis diadema, generates its violet stripe with an unusual type of chromatophore


Nearly all the vibrant blues in animals and plants are created by structural coloration rather than by pigments. However, some types of mandarinfish do possess vesicles of a cyan biochrome of unknown chemical structure in cells named cyanophores.[11] Although they appear unusual in their limited taxonomic range, there may be cyanophores (as well as further unusual chromatophore types) in other fish and amphibians. For example, brightly coloured chromatophores with undefined pigments are found in both poison dart frogs and glass frogs,[15] and atypical dichromatic chromatophores, named erythro-iridophores have been described in Pseudochromis diadema.[16]

Pigment translocation

Fish and frog melanophores are cells that can change colour by dispersing or aggregating pigment-containing bodies.

Many species are able to translocate the pigment inside their chromatophores, resulting in an apparent change in body colour. This process, known as physiological colour change, is most widely studied in melanophores, since melanin is the darkest and most visible pigment. In most species with a relatively thin dermis, the dermal melanophores tend to be flat and cover a large surface area. However, in animals with thick dermal layers, such as adult reptiles, dermal melanophores often form three-dimensional units with other chromatophores. These dermal chromatophore units (DCU) consist of an uppermost xanthophore or erythrophore layer, then an iridophore layer, and finally a basket-like melanophore layer with processes covering the iridophores.[17]

Both types of melanophore are important in physiological colour change. Flat dermal melanophores often overlay other chromatophores, so when the pigment is dispersed throughout the cell the skin appears dark. When the pigment is aggregated toward the centre of the cell, the pigments in other chromatophores are exposed to light and the skin takes on their hue. Likewise, after melanin aggregation in DCUs, the skin appears green through xanthophore (yellow) filtering of scattered light from the iridophore layer. On the dispersion of melanin, the light is no longer scattered and the skin appears dark. As the other biochromatic chomatophores are also capable of pigment translocation, animals with multiple chromatophore types can generate a spectacular array of skin colours by making good use of the divisional effect.[18][19]

A single zebrafish melanophore imaged by time-lapse photography during pigment aggregation

The control and mechanics of rapid pigment translocation has been well studied in a number of different species, in particular amphibians and teleost fish.[20][11] It has been demonstrated that the process can be under hormonal or neuronal control or both. Neurochemicals that are known to translocate pigment include noradrenaline, through its receptor on the surface on melanophores.[21] The primary hormones involved in regulating translocation appear to be the melanocortins, melatonin, and melanin-concentrating hormone (MCH), that are produced mainly in the pituitary, pineal gland, and hypothalamus, respectively. These hormones may also be generated in a paracrine fashion by cells in the skin. At the surface of the melanophore, the hormones have been shown to activate specific G-protein-coupled receptors that, in turn, transduce the signal into the cell. Melanocortins result in the dispersion of pigment, while melatonin and MCH results in aggregation.[22]

Numerous melanocortin, MCH and melatonin receptors have been identified in fish[23] and frogs,[24] including a homologue of MC1R,[25] a melanocortin receptor known to regulate skin and hair colour in humans.[26] It has been demonstrated that MC1R is required in zebrafish for dispersion of melanin.[27] Inside the cell, cyclic adenosine monophosphate (cAMP) has been shown to be an important second messenger of pigment translocation. Through a mechanism not yet fully understood, cAMP influences other proteins such as protein kinase A to drive molecular motors carrying pigment containing vesicles along both microtubules and microfilaments.[28][29][30]

Background adaptation

Most fish, reptiles and amphibians undergo a limited physiological colour change in response to a change in environment. This type of camouflage, known as background adaptation, most commonly appears as a slight darkening or lightening of skin tone to approximately mimic the hue of the immediate environment. It has been demonstrated that the background adaptation process is vision-dependent (it appears the animal needs to be able to see the environment to adapt to it),[31] and that melanin translocation in melanophores is the major factor in colour change.[22] Some animals, such as chameleons and anoles, have a highly developed background adaptation response capable of generating a number of different colours very rapidly. They have adapted the capability to change colour in response to temperature, mood, stress levels, and social cues, rather than to simply mimic their environment.


Transverse section of a developing vertebrate trunk showing the dorsolateral (red) and ventromedial (blue) routes of chromatoblast migration

During vertebrate embryonic development, chromatophores are one of a number of cell types generated in the neural crest, a paired strip of cells arising at the margins of the neural tube. These cells have the ability to migrate long distances, allowing chromatophores to populate many organs of the body, including the skin, eye, ear, and brain. Leaving the neural crest in waves, chromatophores take either a dorsolateral route through the dermis, entering the ectoderm through small holes in the basal lamina, or a ventromedial route between the somites and the neural tube. The exception to this is the melanophores of the retinal pigmented epithelium of the eye. These are not derived from the neural crest. Instead, an outpouching of the neural tube generates the optic cup, which, in turn, forms the retina.

When and how multipotent chromatophore precursor cells (called chromatoblasts) develop into their daughter subtypes is an area of ongoing research. It is known in zebrafish embryos, for example, that by 3 days after fertilization each of the cell classes found in the adult fish — melanophores, xanthophores and iridophores — are already present. Studies using mutant fish have demonstrated that transcription factors such as kit, sox10, and mitf are important in controlling chromatophore differentiation.[32] If these proteins are defective, chromatophores may be regionally or entirely absent, resulting in a leucistic disorder.

Practical applications

In addition to basic research into better understanding of chromatophores themselves, the cells are used for applied research purposes. For example, zebrafish larvae are used to study how chromatophores organise and communicate to accurately generate the regular horizontal striped pattern as seen in adult fish.[33] This is seen as a useful model system for understanding patterning in the evolutionary developmental biology field. Chromatophore biology has also been used to model human condition or disease, including melanoma and albinism. Recently, the gene responsible for the melanophore-specific golden zebrafish strain, Slc24a5, was shown to have a human equivalent that strongly correlates with skin colour.[34]

Chromatophores are also used as a biomarker of blindness in cold-blooded species, as animals with certain visual defects fail to background adapt to light environments.[31] Human homologues of receptors that mediate pigment translocation in melanophores are thought to be involved in processes such as appetite suppression and tanning, making them attractive targets for drugs.[25] Therefore, pharmaceutical companies have developed a biological assay for rapidly identifying potential bioactive compounds using melanophores from the African clawed frog.[35] Other scientists have developed techniques for using melanophores as biosensors,[36] and for rapid disease detection (based on the discovery that pertussis toxin blocks pigment aggregation in fish melanophores).[37] Potential military applications of chromatophore-mediated colour changes have been proposed, mainly as a type of active camouflage, along with invisibility.[38][39]

Cephalopod chromatophores

An infant cuttlefish, using background adaptation to mimic the local environment

Coleoid cephalopods have complex multicellular organs that they use to change colour rapidly. This is most notable in brightly coloured squid, cuttlefish, and octopuses. Each chromatophore unit is composed of a single chromatophore cell and numerous muscle, nerve, glial, and sheath cells.[40] Inside the chromatophore cell, pigment granules are enclosed in an elastic sac, called the cytoelastic sacculus. To change colour the animal distorts the sacculus form or size by muscular contraction, changing its translucency, reflectivity, or opacity. This differs from the mechanism used in fish, amphibians, and reptiles in that the shape of the sacculus is being changed rather than a translocation of pigment vesicles within the cell. However, a similar effect is achieved.

Octopuses can operate chromatophores in complex, wavelike chromatic displays, resulting in a variety of rapidly changing colour schemes.

The nerves that operate the chromatophores are thought to be positioned in the brain in a pattern similar to that of the chromatophores they each control.

This means the pattern of colour change matches the pattern of neuronal activation.

This may explain why, as the neurons are activated one after another, the colour change occurs in waves.[41]

Like chameleons, cephalopods use physiological colour change for social interaction. T

hey are also among the most skilled at background adaptation, having the ability to match both the colour and the texture of their local environment with remarkable accuracy.


Chromatophores are also found in membranes of phototrophic bacteria. Used primarily for photosynthesis, they contain bacteriochlorophyll pigments and carotenoids.[42]

In purple bacteria, such as Rhodospirillum rubrum, the light-harvesting proteins are intrinsic to the chromatophore membranes.

However, in green sulfur bacteria, they are arranged in specialised antenna complexes called chlorosomes.[43]

See also


High Speed Nano-Sized Electronics May be Possible with Chromophores

Published on July 3, 2006 at 12:36 AM

The future of high-speed electronics might very well be defined by linking together small, “electrically jumpy” molecules called chromophores.

According to researchers at the University of Pennsylvania and St. Josephs University, electrical charges can zip along chains of linked chromophores faster than any electrical charge yet observed in organic semiconductors, beating the previous benchmark in this regard by a factor of three.

Their findings suggest the use of chromophore-based circuitry that could create nano-sized electronic components for numerous applications.

Their findings are presented in the current issue of the Journal of the American Chemical Society.

In chemistry, a chromophore is any molecule or part of a molecule responsible for its color.  Light hitting a chromophore excites an electron, which then emits light of a particular color.

“Here we have created chains of chromophores that are primed to move charge,” said Michael J. Therien, a professor in Penn’s Department of Chemistry and lead researcher in the project.

“When a charge is introduced to an array of chromophores linked closely together, it enables electrons to quickly hop from one chromophore to the next.”

A charge can travel down a chain of chromophores at a rate of about 10 million times a second, which means that these chromophore arrays can do anything that organic semiconductors currently do, only much faster.  

Penn researchers Kimihiro Susumu and Paul Frail built chromophore circuits that could, for example, serve as the functional elements in disposable plastic electronics, radio frequency identification tags, electronic drivers for active-matrix liquid crystal displays and organic light-emitting diodes as well as for lightweight solar cells.

Therien and his colleagues have found that the key to creating materials that allow electrons to move so quickly and freely is to build structures that feature long chromophores and short linkers between these units.

“This arrangement of linked chromophores leads to small structural changes when holes (positive charges) and electrons (negative charges) are introduced into these structures and these physical changes help propagate the charge,” said Paul Angiolillo of St. Josephs University, co-author of the study.  

  • “The introduction of these structural changes is actually a new idea in the design of conducting and semi-conducting organic materials.”
  • The semiconductor industry is well aware of potential barriers to creating faster and faster electronics.  In terms of circuitry, size directly relates to speed.
  • Currently, circuits based on semiconductors have shrunk to dimensions just below 100 nanometers, or one hundred billionths of a meter, across.
  • Chromophores may represent the first relatively easy-to-use materials that function on the nanoscale.

“In order to move significantly past the 100-nano barrier in electronics, we need to develop nano structures that let electrons move, as they do through wires and semiconductors,” Therien said.  “Our work also shows for the first time that molecular conductive elements can be produced on a 10-nanometer length scale, providing an important functional element for nanoscale circuitry.


A chromophore is the part of a molecule responsible for its colour. [1] The colour arises when a molecule absorbs certain wavelengths of visible light and transmits or reflects others. The chromophore is a region in the molecule where the energy difference between two different molecular orbitals falls within the range of the visible spectrum. Visible light that hits the chromophore can thus be absorbed by exciting an electron from its ground state into an excited state.

In biological molecules that serve to capture or detect light energy, the chromophore is the moiety that causes a conformational change of the molecule when hit by light.

Chemical structure of beta-carotene. The eleven conjugated double bonds that form the chromophore of the molecule are highlighted in red.

Conjugated pi-bond system chromophores

Conjugated chromophore that straightens in response to a photon γ (light), of the correct wavelength: 11-cis-retinal becomes all-trans-retinal

In the conjugated chromophores, the electrons jump between energy levels that are extended pi orbitals, created by a series of alternating single and double bonds, often in aromatic systems. Common examples include retinal (used in the eye to detect light), various food colorings, fabric dyes (azo compounds), pH indicators, lycopene, β-carotene, and anthocyanins. Various factors in a chromophore’s structure go into determining at what wavelength region in a spectrum the chromophore will absorb. Lengthening or extending a conjugated system with more unsaturated (multiple) bonds in a molecule will tend to shift absorption to longer wavelengths. Woodward-Fieser rules can be used to approximate ultraviolet-visible maximum absorption wavelength in organic compounds with conjugated pi-bond systems.

Some of these are metal complex chromophores, which contain a metal in a coordination complex with ligands. Examples are chlorophyll, which is used by plants for photosynthesis and hemoglobin, the oxygen transporter in the blood of vertebrate animals. In these two examples, a metal is complexed at the center of a tetrapyrrole macrocycle ring: the metal being iron in the heme group (iron in a porphyrin ring) of hemoglobin, or magnesium complexed in a chlorin-type ring in the case of chlorophyll. The highly conjugated pi-bonding system of the macrocycle ring absorbs visible light. The nature of the central metal can also influence the absorption spectrum of the metal-macrocycle complex or properties such as excited state lifetime.[2][3][4] The tetrapyrrole moiety in organic compounds which is not macrocyclic but still has a conjugated pi-bond system still acts as a chromophore. Examples of such compounds include bilirubin and urobilin, which exhibit a yellow color.


An auxochrome is a functional group of atoms attached to the chromophore which modifies the ability of the chromophore to absorb light, altering the wavelength or intensity of the absorption.

Halochromism in chromophores

Halochromism occurs when a substance changes color as the pH changes. This is a property of pH indicators, whose molecular structure changes upon certain changes in the surrounding pH. This change in structure affects a chromophore in the pH indicator molecule. For example, phenolphthalein is a pH indicator whose structure changes as pH changes as shown in the following table:

Structure Phenolphthalein-low-pH-2D-skeletal.svg Phenolphthalein-mid-pH-2D-skeletal.svg
pH 0−8.2 8.2−12.0
Conditions acidic or near-neutral basic
Color name colorless pink to fuchsia

In a pH range of about 0-8, the molecule has three aromatic rings all bonded to a tetrahedral sp3 hybridized carbon atom in the middle which does not make the π-bonding in the aromatic rings conjugate. Because of their limited extent, the aromatic rings only absorb light in the ultraviolet region, and so the compound appears colorless in the 0-8 pH range. However as the pH increases beyond 8.2, that central carbon becomes part of a double bond becoming sp2 hybridized and leaving a p orbital to overlap with the π-bonding in the rings. This makes the three rings conjugate together to form an extended chromophore absorbing longer wavelength visible light to show a fuchsia color.[5] At pH ranges outside 0-12, other molecular structure changes result in other color changes; see Phenolphthalein for details.

See also

External links



The posterior, or part of the body opposite the head, eg. tail in a fish,[1] portion of the corpus callosum is called the splenium; the anterior is called the genu (or “knee”); between the two is the truncus, or “body”, of the corpus callosum. The part between the body and the splenium is often markedly thinned and thus referred to as the “isthmus”. The rostrum is the part of the corpus callosum that projects posteriorly and inferiorly from the anteriormost genu, as can be seen on the sagittal image of the brain displayed on the right. The rostrum is so named for its resemblance to a bird’s beak.

Corpus callosum

Thinner axons in the genu connect the prefrontal cortex between the two halves of the brain, these form a fork-like bundle of fibers known as Forceps Minor. Thicker axons in the midbody of the corpus callosum, known as Trunk, interconnect areas of the premotor and supplementary motor regions and motor cortex, with proportionally more corpus dedicated to supplementary motor regions like Broca’s area. The posterior body of the corpus, known as splenium, communicates somatosensory information between the two halves of the parietal lobe and visual center at the occipital lobe, these fibers are known as Forceps Major.[2][3]


Agenesis of the corpus callosum (ACC) is a rare congenital disorder in which the corpus callosum is partially or completely absent. ACC is usually diagnosed within the first two years of life and may manifest as a severe syndrome in infancy or childhood, as a milder condition in young adults, or as an asymptomatic incidental finding. Initial symptoms of ACC usually include seizures, which may be followed by feeding problems and delays in holding the head erect, sitting, standing, and walking. Other possible symptoms may include impairments in mental and physical development, hand-eye coordination, and visual and auditory memory. Hydrocephaly may also occur. In mild cases, symptoms such as seizures, repetitive speech, or headaches may not appear for years.

ACC is usually non-fatal. Treatment usually involves management of symptoms, such as hydrocephaly and seizures, if they occur. Although many children with the disorder will lead normal lives and have average intelligence, careful neuropsychological testing reveals subtle differences in higher cortical function compared to individuals of the same age and education without ACC. Children with ACC accompanied by developmental delay and/or seizure disorders should be screened for metabolic disorders.[4]

In addition to agenesis of the corpus callosum, similar conditions are hypogenesis (partial formation), dysgenesis (malformed), and hypoplasia (underdevelopment, including too thin).

Recent studies have also linked possible correlations between corpus callosum malformation and autism spectrum disorders (ASD).[5]

Kim Peek, a savant and the inspiration behind the movie Rain Man, was found with agenesis of the corpus callosum.

Sexual dimorphism

The corpus callosum and its relation to sex has been a subject of debate in the scientific and lay communities for over a century. Initial research in the early 20th century claimed the corpus to be different in size between men and women. That research was in turn questioned, and ultimately gave way to more advanced imaging techniques that appeared to refute earlier correlations. The new advent of physiologic based imaging has altered the paradigm dramatically, with the relationship between gender and the corpus callosum becoming a subject of increasing numbers of studies in recent years.[citation needed]


Physiologic imaging

The ability to evaluate the form and function of the human mind has undergone almost exponential growth and a paradigm shift in recent years. Magnetic resonance imaging, for example, is now being used to analyze physiology in addition to anatomy. Using diffusion tensor sequences on MRI machines, the rate that molecules diffuse in and out of a specific area of tissue, directionality or anisotropy, and rates of metabolism can be measured. These sequences have found consistent sex differences in human corpus callosal morphology and microstructure.[which?][6][7][8]

Morphometric analysis has also been used to study specific 3-dimensional mathematical relationships with MRIs, and have found consistent and statistically significant differences across genders.[9][10] Specific algorithms have found significant gender differences in over 70% of cases in one review.[11]

Gender identity disorder

Research has been done on the shape of the corpus callosum in those with gender identity disorder. Researchers were able to demonstrate that the shape dimorphism of the corpus callosum at birth in biological males who self-identified as female was actually reversed, and that the same held true for biological females who self-identified as male. The publishers of this article argued that the shape of the corpus callosum defined the mental sex of individuals over their physical sex.[11]

The relationship between the corpus callosum and gender remains an active subject of debate in the scientific and lay community.

Other correlations

The front portion of the corpus callosum has been reported to be significantly larger in musicians than non-musicians,[12] and to be 0.75 square centimeters [13] or 11% larger in left-handed and ambidextrous people than right-handed people.[13][14] This difference is evident in the anterior and posterior regions of the corpus callosum but not in the splenium.[13] Other magnetic resonance morphometric study showed that corpus callosum size correlates positively with verbal memory capacity and semantic coding test performance.[15] Research has shown that children with dyslexia tend to have smaller and less developed corpus callosums than their non-dyslexic counterparts.[16][17]

Musical training has shown to increase plasticity of the corpus callosum during a sensitive period of time in development. The implications are an increased coordination of hands, differences in white matter structure, and amplification of plasticity in motor and auditory scaffolding which would serve to aid in future musical training. The study found children who had begun musical training before the age of six (minimum 15 months of training) had an increased volume of their corpus callosum and adults who had begun musical training before the age of 11 also had increased bi-manual coordination.[18]

Clinical significance


Electroencephalography is used to find the source of electrical activity causing a seizure as part of the surgical evaluation for a corpus callosotomy.

The symptoms of refractory epilepsy can be reduced by cutting the corpus callosum in an operation known as a corpus callosotomy.[19] This is usually reserved for cases in which complex or grand mal seizures are produced by an epileptogenic focus on one side of the brain, causing an interhemispheric electrical storm. The work up for this procedure involves an electroencephalogram, MRI, PET scan, and evaluation by a specialized neurologist, neurosurgeon, psychiatrist, and neuroradiologist before surgery can be considered.[20]

Other disease

Anterior corpus callosum lesions may result in akinetic mutism or tactile anomia. Posterior corpus callosum (splenium) lesions may result in alexia without agraphia.

See Also:

Brain split procedure

The cerebral cortex is divided into two hemispheres and is connected by the corpus callosum. A procedure that helps patients to alleviate the severity of seizures is called split brain procedure. The result is that a seizure that starts in one hemisphere is isolated in that hemisphere since there is no longer a connection to the other side. However, this procedure is dangerous and risky.


The first study of the corpus with relation to gender was by R. B. Bean, a Philadelphia anatomist, who suggested in 1906 that “exceptional size of the corpus callosum may mean exceptional intellectual activity” and that there were measurable differences between men and women. Perhaps reflecting the political climate of the times, he went on to claim differences in the size of the callosum across different races. His research was ultimately refuted by Franklin Mall, the director of his own laboratory.[21]

Of more mainstream impact was a 1982 Science article by Holloway and Utamsing that suggested sex difference in human brain morphology, which related to differences in cognitive ability.[22] Time published an article in 1992 that suggested that, because the corpus is “often wider in the brains of women than in those of men, it may allow for greater cross-talk between the hemispheres—possibly the basis for women’s intuition.”[23]

More recent publications in the psychology literature have raised doubt as to whether the anatomic size of the corpus is actually different. A meta-analysis of 49 studies since 1980 found that, contrary to de Lacoste-Utamsing and Holloway, no sex difference could be found in the size of the corpus callosum, whether or not account was taken of larger male brain size.[21] A study in 2006 using thin slice MRI showed no difference in thickness of the corpus when accounting for the size of the subject.[24]

In other animals

The corpus callosum is found only in placental mammals (the eutherians), while it is absent in monotremes and marsupials,[25] as well as other vertebrates such as birds, reptiles, amphibians and fish.[26] (Other groups do have other brain structures that allow for communication between the two hemispheres, such as the anterior commissure, which serves as the primary mode of interhemispheric communication in marsupials,[27][28] and which carries all the commissural fibers arising from the neocortex(also known as the neopallium), whereas in placental mammals the anterior commissure carries only some of these fibers.[29]) In primates, the speed of nerve transmission depends on its degree of myelination, or lipid coating. This is reflected by the diameter of the nerve axon. In most primates, axonal diameter increases in proportion to brain size to compensate for the increased distance to travel for neural impulse transmission. This allows the brain to coordinate sensory and motor impulses. However, the scaling of overall brain size and increased myelination has not occurred between chimpanzees and humans. This has resulted in the human corpus callosum’s requiring double the time for interhemispheric communication as a macaque‘s.[2]

Sagittal post-mortem section through the midline brain. The corpus callosum is the curved band of lighter tissue at the center of the brain above the hypothalamus. Its lighter texture is due to higher myelin content, resulting in faster neuronal impulse transmission.

The fibrous bundle that the corpus callosum appears as, can and does increase to such an extent in humans that it encroaches upon and wedges apart the hippocampal structures.[30]

Additional images

About Timothytrespas

I am a victim of human experimentation MK-ultra mind control Morgellons nanotechnology syndrome & remote neural connectivity. I am an artist, inventor, musician, thinker, lover, human being who cares for all humanity & all life. I believe people should endeavor to live in peaceful cooperation rather than brutal waring survival of the most brutal. We live in a forced false-paradigm and I desire to wake people up from the 'trance hypnotic mind control programming' to the 'TRUTH of light and love'! Blessing and peace. Justice to all who suffer under tyranny. Compassion for all beings. May GOD have mercy on us all.
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