Instead of a six-layer neocortex or a cluster of nuclei, the turtle brain had layer 4- and 5-like cells distributed along a single layer of the species' dorsal cortex.
Future experiments will test the developmental steps that shape these neurons into various structures, and the relative pros and cons of these anatomical differences. The complex language and tool-use of some bird species suggests that the nuclear organization of this pathway is also capable of supporting advanced functions -- and even may offer advantages over the mammalian brain. It's as if you have additional flexibility: You can have shorter circuits, longer circuits, you can have specialized processing centers.
Beyond the structural differences, the discovery of homologous neocortex cell types will allow scientists to study cortical neurons in bird species such as the chicken, a common model used for examining embryonic development. Such research could help scientists more easily study the neurons lost in paralysis, deafness, blindness, and other neurological conditions. Materials provided by University of Chicago Medical Center. Note: Content may be edited for style and length. Science News. Rowell, and Clifton W. Cell-type homologies and the origins of the neocortex.
ScienceDaily, 1 October Moreover, the differences in expression between human and chimpanzee brain tissue mirrored the differences found in cells transfected with human FOXP2 or chimpanzee FOXP2. GO analysis of differentially expressed genes in the brain showed an enrichment of categories related to tissue and organ development and cell—cell signaling. As a gene associated with a human-specific trait, FOXP2 would at first glance seem to be a dream come true for evolutionary geneticists. Moreover, it is hard not to be impressed by the depth and breadth of the research related to FOXP2.
Nevertheless, there is still no clear or direct connection between the human-specific amino acid substitutions in FOXP2 and speech. The fact that mutations of FOXP2 in humans result in speech impairments shows that it plays a role in speech development, but the nature of its role remains unclear. It might play a very specific role, for example, by orchestrating a whole set of genes that switch brain development from an ancestral program to a human program that causes cells and connections to differentiate into systems that sustain speech or language.
It might even regulate the development of other parts of the anatomy, such as the lungs and larynx, involved in speech production. Alternatively, FOXP2 might have a permissive role, for example, by regulating some aspects of cell behavior required for the normal development of language systems, but also for the normal development of other structures and systems. In neither case, however, do we have a direct connection between language and the specific FOXP2 substitutions that took place in human evolution TN and NS.
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There is not much question that these changes were the result of selection, and that they affect gene expression in the brain. However, given the widespread pattern of FOXP2 gene expression in the body, those substitutions are likely to affect gene expression in other organs, so it remains possible that the substitutions were driven by selection acting on non—speech-related parts of the brain or nonbrain tissues and organs.
Humans are, after all, not just apes with unusually large, complex brains: other aspects of anatomy and physiology were extensively modified in human evolution as well. It could also be the case that FOXP2 has a speech- or language-specific function in the human brain, by virtue of the action of other transcription factors that bind to the same promoters in brain cells targeted by human FOXP2.
However, then we would be talking about the interactions of genes involved in building a human organism, rather than a single gene, and it still would not be clear, without additional evidence, that the amino acid substitutions in FOXP2 were selected for their effects on developmental pathways specific to language. It would seem that the crux of the problem with tying FOXP2 to language is that we are trying to relate a multifunctional gene to a complex, high-level phenotype, by which I mean a phenotype that encompasses a diverse collection of tissues and cell types.
It is probably not realistic to think that the development of such systems has simple genetic triggers and they are the products of epigenetic programs acting in isolation from other epigenetic programs. This conclusion merely restates two of the important lessons of experimental population genetics: first, that most phenotypes arise through the interactions of multiple genes the principle of epistasis , and, second, that most genes influence multiple phenotypes the principle of pleiotropy Mayr, ; Dobzhansky et al.
These considerations, along with the great number and variety of human genetic specializations, make it unlikely that evolutionary changes in just a few regulatory genes, acting early in development, can explain most of the phenotypic differences between humans and chimpanzees, as King and Wilson and Gould suggested. There might, in fact, be a relatively small number of genes that do act early in development and do have profound effects, but as we have seen with FOXP2 , the genes downstream of a regulatory gene themselves can undergo evolutionary changes Spiteri et al.
Without a deeper understanding of development and, especially, of the human-specific aspects of human development, we are not likely to be able to make many definite connections between high-level phenotypes and the role of early-acting regulatory genes.
This raises a matter of serious concern: our lack of direct information about the human organism. I have noted the lack of detailed accounts of the human neurobiological and psychological phenotypes, and I think it would be fair to say we are quite ignorant about many other human--specific features of human biology, including human-specific modifications of the developmental programs that generate human-specific phenotypes.
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In part, this lack of knowledge reflects technical limitations to our ability to study humans: just as we cannot do invasive neurobiological investigations, we cannot do invasive or terminal developmental investigations or transgenic experiments either. Given this, it is not surprising that we rely so much on studies of model animals to understand normal human biology and its development, with the hope that there is enough commonality in epigenetic systems across species that results in models will translate to humans.
This approach seems particularly problematic when human-specific phenotypes are at issue. Presumably, no one expected that expressing human FOXP2 in a mouse would yield a mouse that talks. It is, after all, a human gene on a mouse background, and without understanding the similarities and differences between human and mouse developmental programs, predictions about the specific effects of a mutant human gene on the high-level phenotypes of mice are hazardous.
In offering this critique, I do not mean to say that mouse models are not useful or informative, but rather that they are not enough by themselves. Certainly, every aspect of our science would benefit from the better characterization of human-specific phenotypes, and the most direct way to obtain that information, especially for high-level phenotypes, is by studying humans directly.
However, we do need other experimental paradigms to help us explore the phenotypic consequences of human-specific genetic changes. Investigations of gene functions in cell culture, as exemplified by a number of the studies cited earlier, provide another avenue for empirical research. This approach could be further empowered. How this works is illustrated by the studies reviewed in the previous section showing that FOXP2 expression affects neurite outgrowth and synaptic plasticity Vernes et al. There are additional lines of evidence suggesting that evolution targeted these features of human neuronal biology.
It is noteworthy, too, that there is genomic evidence for positive selection on genes.