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Category Archives: chimpanzee

Astrocytes: a key "wiring" element behind human intelligence

Recent experiments with mice have shown that those with transplanted human glial cells known as astrocytes perform much better in learning and memory tests afterwards.
Xiaoning Han et al., Forebrain Engraftment by Human Glial Progenitor Cells Enhances Synaptic Plasticity and Learning in Adult Mice. Stem Cell 2013. Pay per viewLINK [doi:10.1016/j.stem.2012.12.015]
See the news article at Science Daily for details. 
One wonders if they gave mice some sort of humanity and the many ethical questions behind this experiment, of course. But what got me wondering after that is do chimpanzees have the same kind of astrocytes as we do?
And the answer seems to be yes but no.
Nancy A. Oberheim et al., Uniquely Hominid Features of Adult Human Astrocytes. The Journal of Neuroscience 2009. Freely accessibleLINK [doi:10.1523/​JNEUROSCI.4707-08.2009]
Chimpanzees and humans share a type of astrocytes not found in our monkey or rodent relatives but the density and complexity of these particular glial cells in humans is much greater than in chimpanzees.

Fig 2 (legend)

One of the most striking features distinguishing humans and chimpanzee from other lower primate and rodent astrocytes was the presence of a previously undescribed pool of morphologically distinct GFAP+ cells residing in layers 5–6, characterized by long fibers with prominent varicosities (Fig. 2A). (…) In our analysis of primate tissue, we were able to locate a small number of varicose projection astrocytes within layers 5 or 6 of the chimpanzee cortex (Fig. 2A, inset). These cells differed from those seen in human in that they were smaller and less complex, with fewer main GFAP+ processes.

This is not the only difference, another subgroup, the interlaminar astrocytes also shows differences:

In addition to being more numerous than their chimpanzee counterparts, the morphology of interlaminar astrocytes is subtly different in humans. Human interlaminar astrocytes have small spheroid cell bodies and several short processes that contribute to the pial glial limitains, creating a thick network of GFAP fibers not seen in the primate.

A third category, the protoplasmatic astrocytes, is also different:

… the average diameter of protoplasmic cortical astrocytes in the chimpanzee brain was 81.7 ± 1.9 μm (n = 36), which is significantly smaller than human astrocytes, but significantly larger than protoplasmic astrocytes in mouse brain…

So what about cetaceans, which include some of the non-human animals most famed for their intellectual capabilities? The brain structure seems different, so maybe not as easy to compare as with our closest relatives, also cetaceans do not seem so well researched. But we know (source) that at least that the proportion of glial cells in bottlenose dolphin forebrains is almost double than that of humans:

Glial cells outnumber neurons by at least 6 to 1 but the ratio differs
in different parts of the nervous system. The ratio can be 100 glials to
1 neuron along nerves in the white matter tracts in the brain; in the
frontal cortex the ratio is 4 to 1. Interestingly, whales and dolphins
have 7 glials for every neuron in their gigantic forebrains. (Fields, R.
Douglas, PhD. The Other Brain. P P 24. NY:Simon & Schuster, 2009.)

 
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Posted by on March 9, 2013 in chimpanzee, dolphin, human evolution, mind

 

Chromosome scale evolution among Hominidae (great apes, humans)

I won’t surely be able to make justice here to this most interesting but highly technical paper but mention must be done of it in any case:
Marta Farré et al., Recombination Rates and Genomic Shuffling in Human and Chimpanzee—A New Twist in the Chromosomal Speciation Theory. Molecular Biology and Evolution, 2012. Open accessLINK [doi: 10.1093/molbev/mss272]

Abstract

A long-standing question in evolutionary biology concerns the effect of recombination in shaping the genomic architecture of organisms and, in particular, how this impacts the speciation process. Despite efforts employed in the last decade, the role of chromosomal reorganizations in the human–chimpanzee speciation process remains unresolved. Through whole-genome comparisons, we have analyzed the genome-wide impact of genomic shuffling in the distribution of human recombination rates during the human–chimpanzee speciation process. We have constructed a highly refined map of the reorganizations and evolutionary breakpoint regions in the human and chimpanzee genomes based on orthologous genes and genome sequence alignments. The analysis of the most recent human and chimpanzee recombination maps inferred from genome-wide single-nucleotide polymorphism data revealed that the standardized recombination rate was significantly lower in rearranged than in collinear chromosomes. In fact, rearranged chromosomes presented significantly lower recombination rates than chromosomes that have been maintained since the ancestor of great apes, and this was related with the lineage in which they become fixed. Importantly, inverted regions had lower recombination rates than collinear and noninverted regions, independently of the effect of centromeres. Our observations have implications for the chromosomal speciation theory, providing new evidences for the contribution of inversions in suppressing recombination in mammals. 

Maybe most interesting, at least for the casual reader, is this graph:

Fig. 1.

Evolutionary history of human chromosomes superimposed on the phylogeny of great apes. Black lines within the phylogenetic tree represent the ancestral state of the chromosomes, whereas red and orange lines represent the rearranged forms. Orangutan maintains the ancestral form for orthologous chromosomes 3 and 11, whereas human, chimpanzee, and gorilla forms are derived. Orthologous chromosomes 1, 2, and 18 have been rearranged in the lineage leading to humans, whereas orthologous chromosomes 4, 9, 15, 16, and 17 are rearranged in the lineage leading to chimpanzee. Ancestral chromosome 5 has been maintained in orangutan and human but has suffered two independent inversions in chimpanzee and gorilla, respectively. Chromosome 7 has suffered one inversion, which has been fixed in gorilla, and another inversion has been fixed in the lineage leading to human and chimpanzee. Chromosome 10 underwent one inversion that was fixed in human and chimpanzee, and a new inversion fixed in gorilla. Finally, chromosome 12 has maintained the ancestral form in humans and orangutans but has undergone an inversion that has been fixed in chimpanzee and gorilla, therefore, the polymorphic state has persisted across multiple speciation nodes (gorilla–human–chimpanzee and human–chimp).

large original version

No changes at this scale happened in the other eight autosomes (6, 8, 13, 14, 19, 20, 21, and 22) in any of the four genera. 
Warning must be done about the timeline, which should be twice as old at least for the Pan-Homo split.
It is interesting to notice that Pan (chimpanzee) and Gorilla share a derived form of the chromosome 12, indicating that the Homininae split was not too clean, possibly with gorilla introgression into chimpanzees. 
It is also interesting to realize that orangutans (Pongo) are extremely conservative in the genome (all 22 chromosomes, what means that surely the common ancestor of all Hominidae was more similar to modern orangutans than to any other branch. 
Finally I find notable that our chimpanzee cousins are actually more evolved than us, literally, a blunt numerical truth that is strongly counterintuitive for our anthropocentric vision of biology and evolution. While us humans have conserved 15 ancestral chromosomes (almost as many as gorillas: 16), chimpanzees only conserved 11, evolving one step (red lines) 9 chromosomes (humans 6, gorillas 5) and two steps (orange lines) two chromosomes (humans and gorillas just one).

PS- On the other hand, our Homo branch has a peculiar chromosomal rearrangement that puts up quite apart from the rest of Hominidae: two ancestral chromosomes got fused into a single one (chromosome 2) in our line. This may well have been decisive in our reproductive divergence from Pan and even maybe Gorilla, crafting a very impassable biological barrier. (Not in the paper, just my afterthought).

Incidentally, a 2006 study (Wainwright 2006) claimed to have found some strong correlation between cognitive abilities (not just IQ but also other more creative aspects of the mind) and areas of chromosome 2. With the usual caution I guess it is worth mentioning here.

 
 

Hominid speciation: sudden or gradual?

It depends apparently: bonobos may have diverged quite suddenly while in other cases, including the Pan-Homo split, the process of speciation appears to have been more gradual.

Thomas Mailund et al., A New Isolation with Migration Model along Complete Genomes Infers Very Different Divergence Processes among Closely Related Great Ape Species. PLoS ONE 2012. Open access LINK [doi:10.1371/journal.pgen.1003125]

Abstract

We present a hidden Markov model (HMM) for inferring gradual isolation
between two populations during speciation, modelled as a time interval
with restricted gene flow. The HMM describes the history of adjacent
nucleotides in two genomic sequences, such that the nucleotides can be
separated by recombination, can migrate between populations, or can
coalesce at variable time points, all dependent on the parameters of the
model, which are the effective population sizes, splitting times,
recombination rate, and migration rate. We show by extensive simulations
that the HMM can accurately infer all parameters except the
recombination rate, which is biased downwards. Inference is robust to
variation in the mutation rate and the recombination rate over the
sequence and also robust to unknown phase of genomes unless they are
very closely related. We provide a test for whether divergence is
gradual or instantaneous, and we apply the model to three key divergence
processes in great apes: (a) the bonobo and common chimpanzee, (b) the
eastern and western gorilla, and (c) the Sumatran and Bornean
orang-utan. We find that the bonobo and chimpanzee appear to have
undergone a clear split, whereas the divergence processes of the gorilla
and orang-utan species occurred over several hundred thousands years
with gene flow stopping quite recently. We also apply the model to the Homo/Pan speciation event and find that the most likely scenario involves an extended period of gene flow during speciation.

 
 

Latest genetic news (links)

Anthropological and genetic news have been piling up in this strike journey. I’m not sure if I will be able to address all as they may deserve so I’m listing them here in very quick review.
My apologies because I meant that the “links” format would be over but if people overseas (and in some cases also in Europe) insist on working in the general strike journey and publishing things all around, all I can do is this (or risking not even doing anything at all).

Chimpanzee enterotype variation is just like ours. 

Even if our genomes have diverged the microscopic environments we host in our guts are almost exactly the same, with three different types depending exclusively on diet.
Andrew H. Moeller et al., Chimpanzees and humans harbour compositionally similar gut enterotypes. Nature Communications, 2012. Pay per view ··> LINK [doi:10.1038/ncomms2159]

Abstract

Microbes inhabiting the human gastrointestinal tract tend to adopt one of three characteristic community structures, called ‘enterotypes’, each of which is overrepresented by a distinct set of bacterial genera. Here we report that the gut microbiotae of chimpanzees also assort into enterotypes and that these chimpanzee enterotypes are compositionally analogous to those of humans. Through the analysis of longitudinal samples, we show that the microbial signatures of the enterotypes are stable over time, but that individual hosts switch between enterotypes over periods longer than a year. These results support the hypothesis that enterotypic variation was present in populations of great apes before the divergence of humans and chimpanzees.

A more detailed review can be found at John Hawks’ Weblog.

Fig. 1 (a) Left chimpanzee enterotypes, right human ones

High altitude adaptions in Ethiopia

Research on Ethiopian genetic nuances with a Basque name as lead researcher:
Gorka Alkorta Aranburu et al., The genetic architecture of adaptations (sic) to high altitude in Ethiopia. Pre-pub at arXiv, 2012. Freely accessible ··> LINK [ref. code:
arXiv:1211.3053 [q-bio.PE]]

Abstract


Although hypoxia is a major stress on physiological processes, several human
populations have survived for millennia at high altitudes, suggesting that they
have adapted to hypoxic conditions. This hypothesis was recently corroborated
by studies of Tibetan highlanders, which showed that polymorphisms in candidate
genes show signatures of natural selection as well as well-replicated
association signals for variation in hemoglobin levels. We extended genomic
analysis to two Ethiopian ethnic groups: Amhara and Oromo. For each ethnic
group, we sampled low and high altitude residents, thus allowing genetic and
phenotypic comparisons across altitudes and across ethnic groups. Genome-wide
SNP genotype data were collected in these samples by using Illumina arrays. We
find that variants associated with hemoglobin variation among Tibetans or other
variants at the same loci do not influence the trait in Ethiopians. However, in
the Amhara, SNP rs10803083 is associated with hemoglobin levels at genome-wide
levels of significance. No significant genotype association was observed for
oxygen saturation levels in either ethnic group. Approaches based on allele
frequency divergence did not detect outliers in candidate hypoxia genes, but
the most differentiated variants between high- and lowlanders have a clear role
in pathogen defense. Interestingly, a significant excess of allele frequency
divergence was consistently detected for genes involved in cell cycle control,
DNA damage and repair, thus pointing to new pathways for high altitude
adaptations. Finally, a comparison of CpG methylation levels between high- and
lowlanders found several significant signals at individual genes in the Oromo. 

An extensive review can be found at Ethio Helix (where else?)

Pig and boar genomes and evolutionary history

Martien A.M. Groenen et al., Analyses of pig genomes provide insight into porcine demography and evolution. Nature 2012. Open access ··> LINK [doi:10.1038/nature11622]

Abstract

For 10,000years pigs and humans have shared a close and complex relationship. From domestication to modern breeding practices, humans have shaped the genomes of domestic pigs. Here we present the assembly and analysis of the genome sequence of a female domestic Duroc pig (Sus scrofa) and a comparison with the genomes of wild and domestic pigs from Europe and Asia. Wild pigs emerged in South East Asia and subsequently spread across Eurasia. Our results reveal a deep phylogenetic split between European and Asian wild boars ~1 million years ago, and a selective sweep analysis indicates selection on genes involved in RNA processing and regulation. Genes associated with immune response and olfaction exhibit fast evolution. Pigs have the largest repertoire of functional olfactory receptor genes, reflecting the importance of smell in this scavenging animal. The pig genome sequence provides an important resource for further improvements of this important livestock species, and our identification of many putative disease-causing variants extends the potential of the pig as a biomedical model.

Fig. 3 – reconstructed/estimated demographic history of boars

Less obvious strategies in long term evolutionary co-adaption

Interesting read on how competition can cause the formation of deep evolutionary valleys or gorges from which it is most difficult to exit and are therefore evolutionarily stable.
Eric Chastain et al., Defensive complexity and the phylogenetic conservation of immune control. Pre-pub at arXiv, 2012. Freely accessible ··> LINK [ref code: arXiv:1211.2878 [q-bio.PE]]

Abstract

One strategy for winning a coevolutionary struggle is to evolve rapidly. Most of the literature on host-pathogen coevolution focuses on this phenomenon, and looks for consequent evidence of coevolutionary arms races. An alternative strategy, less often considered in the literature, is to deter rapid evolutionary change by the opponent. To study how this can be done, we construct an evolutionary game between a controller that must process information, and an adversary that can tamper with this information processing. In this game, a species can foil its antagonist by processing information in a way that is hard for the antagonist to manipulate. We show that the structure of the information processing system induces a fitness landscape on which the adversary population evolves. Complex processing logic can carve long, deep fitness valleys that slow adaptive evolution in the adversary population. We suggest that this type of defensive complexity on the part of the vertebrate adaptive immune system may be an important element of coevolutionary dynamics between pathogens and their vertebrate hosts. Furthermore, we cite evidence that the immune control logic is phylogenetically conserved in mammalian lineages. Thus our model of defensive complexity suggests a new hypothesis for the lower rates of evolution for immune control logic compared to other immune structures. 

Genetics and psychology in relation to heroin use and abuse

Ting Li et al., Pathways to Age of Onset of Heroin Use: A Structural Model Approach Exploring the Relationship of the COMT Gene, Impulsivity and Childhood Trauma. PLoS ONE, 2012. Open access ··> LINK [doi:10.1371/journal.pone.0048735] 

Abstract

Background

The interaction of the association of dopamine genes, impulsivity and childhood trauma with substance abuse remains unclear.

Objectives

To
clarify the impacts and the interactions of the Catechol
-O-methyltransferase (COMT) gene, impulsivity and childhood trauma on
the age of onset of heroin use among heroin dependent patients in China.

Methods

202
male and 248 female inpatients who meet DSM-IV criteria of heroin
dependence were enrolled. Impulsivity and childhood trauma were measured
using BIS-11 (Barratt Impulsiveness Scale-11) and ETISR-SF (Early
Trauma Inventory Self Report-Short Form). The single nucleotide
polymorphism (SNP) rs737866 on the COMT gene-which has previously been
associated with heroin abuse, was genotyped using a DNA sequence
detection system. Structural equations model was used to assess the
interaction paths between these factors and the age of onset of heroin
use.

Principal Findings

Chi-square
test indicated the individuals with TT allele have earlier age of onset
of heroin use than those with CT or CC allele. In the correlation
analysis, the severity of childhood trauma was positively correlated to
impulsive score, but both of them were negatively related to the age of
onset of heroin use. In structure equation model, both the COMT gene and
childhood trauma had impacts on the age of onset of heroin use directly
or via impulsive personality.

Conclusions

Our
findings indicated that the COMT gene, impulsive personality traits and
childhood trauma experience were interacted to impact the age of onset
of heroin use, which play a critical role in the development of heroin
dependence. The impact of environmental factor was greater than the COMT
gene in the development of heroin dependence.

 

Variation in human (modern and archaic) and chimpanzee lipoprotein APOE

This new study has some interest in understanding some details, of metabolic relevance, of the genetics of humans and our closest relatives:
Annick McIntosh et al., The Apolipoprotein E (APOE) Gene Appears Functionally Monomorphic in Chimpanzees (Pan troglodytes). PLoS ONE 2012. Open access ··> LINK [doi:10.1371/journal.pone.0047760]

Abstract

Background

The human apolipoprotein E (APOE) gene is polymorphic, with three primary alleles (E2, E3, E4) that differ at two key non-synonymous sites. These alleles are functionally different in how they bind to lipoproteins, and this genetic variation is associated with phenotypic variation for several medical traits, including cholesterol levels, cardiovascular health, Alzheimer’s disease risk, and longevity. The relative frequencies of these alleles vary across human populations, and the evolution and maintenance of this diversity is much debated. Previous studies comparing human and chimpanzee APOE sequences found that the chimpanzee sequence is most similar to the human E4 allele, although the resulting chimpanzee protein might function like the protein coded for by the human E3 allele. However, these studies have used sequence data from a single chimpanzee and do not consider whether chimpanzees, like humans, show intra-specific and subspecific variation at this locus.

Methodology and Principal Findings

To examine potential intraspecific variation, we sequenced the APOE gene of 32 chimpanzees. This sample included 20 captive individuals representing the western subspecies (P. troglodytes verus) and 12 wild individuals representing the eastern subspecies (P. t. schweinfurthii). Variation in our resulting sequences was limited to one non-coding, intronic SNP, which showed fixed differences between the two subspecies. We also compared APOE sequences for all available ape genera and fossil hominins. The bonobo APOE protein is identical to that of the chimpanzee, and the Denisovan APOE exhibits all four human-specific, non-synonymous changes and appears functionally similar to the human E4 allele.

Conclusions

We found no coding variation within and between chimpanzee populations, suggesting that the maintenance of functionally diverse APOE polymorphisms is a unique feature of human evolution.

The relevant details are all in table 1:

Table 1. Variation at key APOE functional sites in Homo and Pan.
There is uncertainty about the correctness of the only known Neanderthal triplet.
Even if E4 seems to be the ancestral type, E3 is the most common allele in our species, ranging from 50% in most populations to as much as 90% among some tribes.
 

Some chimp-human differences are epigenetic

Nothing related to brain function this time but rather to attributes that our jungle cousins seem to be at advantage compared to us. Notably chimpanzees almost never have cancer or some other diseases, like mental disorders, which we suffer a lot. This new research suggests it may be because of low methylation levels in humans (i.e. epigenetics, hinting at environmental causes rather than pure inheritance).
Jia Zeng et al., Divergent Whole-Genome Methylation Maps of Human and Chimpanzee Brains Reveal Epigenetic Basis of Human Regulatory Evolution. AJHG 2012. Pay per view (free after 6 months embargo) ··> LINK [doi:10.1016/j.ajhg.2012.07.024]

Abstract

DNA methylation is a pervasive epigenetic DNA modification that strongly affects chromatin regulation and gene expression. To date, it remains largely unknown how patterns of DNA methylation differ between closely related species and whether such differences contribute to species-specific phenotypes. To investigate these questions, we generated nucleotide-resolution whole-genome methylation maps of the prefrontal cortex of multiple humans and chimpanzees. Levels and patterns of DNA methylation vary across individuals within species according to the age and the sex of the individuals. We also found extensive species-level divergence in patterns of DNA methylation and that hundreds of genes exhibit significantly lower levels of promoter methylation in the human brain than in the chimpanzee brain. Furthermore, we investigated the functional consequences of methylation differences in humans and chimpanzees by integrating data on gene expression generated with next-generation sequencing methods, and we found a strong relationship between differential methylation and gene expression. Finally, we found that differentially methylated genes are strikingly enriched with loci associated with neurological disorders, psychological disorders, and cancers. Our results demonstrate that differential DNA methylation might be an important molecular mechanism driving gene-expression divergence between human and chimpanzee brains and might potentially contribute to the evolution of disease vulnerabilities. Thus, comparative studies of humans and chimpanzees stand to identify key epigenomic modifications underlying the evolution of human-specific traits.

See also the article at Science Daily.

 

Increased complexity in certain regions sets apart human and chimp brains

Frontal lobe (CC-BY-SA-2.1-jp)
This paper looks like a very important research piece for the understanding of the human mind, of what makes our brains specifically human and ultimately of what makes ourselves what we are.
Genevieve Konopka et al., Human-Specific Transcriptional Networks in the Brain. Neuron 2012. (Freely accessible apparently) ··> LINK [doi:10.1016/j.neuron.2012.05.034]

Summary

Understanding human-specific patterns of brain gene expression and
regulation can provide key insights into human brain evolution and
speciation. Here, we use next-generation sequencing, and Illumina and
Affymetrix microarray platforms, to compare the transcriptome of human,
chimpanzee, and macaque telencephalon. Our analysis reveals a
predominance of genes differentially expressed within human frontal lobe
and a striking increase in transcriptional complexity specific to the
human lineage in the frontal lobe. In contrast, caudate nucleus gene
expression is highly conserved. We also identify gene coexpression
signatures related to either neuronal processes or neuropsychiatric
diseases, including a human-specific module with CLOCK as its hub gene and another module enriched for neuronal morphological processes and genes coexpressed with FOXP2,
a gene important for language evolution. These data demonstrate that
transcriptional networks have undergone evolutionary remodeling even
within a given brain region, providing a window through which to view
the foundation of uniquely human cognitive capacities.

Hippocampus (CC-BY-SA-2.1-jp)
For what I could understand, mostly from the press release, the authors unveiled increased complexity of the gene expression modulating three regions of our brains: the frontal cortex, the hippocampus and the striatum.
It is not a mere matter of size but specially one of much increased complexity in the wiring of these three regions what seems to make our brains unique. 
The research also reinforces the apparent importance of the much debated genes CLOCK (affecting circadian rhythms, mood, pregnancy and metabolism), FOXP1 and FOXP2 (related specially with speech), whose connectivity is much increased in humans in comparison with our ape cousins.