What is the difference between human and chimpanzee characteristics

For example, when we think about what are the measures that allow us to examine how we may have evolved, we can use genetic information. Sometimes we obtain postmortem brain tissue from our closest ancestral relatives. We can measure the magnitude of gyrations in the cortex and explore specific ideas or hypotheses about how they may be important. In addition, we have fossil crania to study and, from those skulls, we can build casts or make CT scans to get an idea of how the brain size was changing, again building our theories based on these measurements and the correlations that exist.

Furthermore, we have cultural icons as well that give us an idea of how far a species had emerged, given its ability to build, plan, and generate art. In each case, we have material that we can work with: genetic material, tissues, organs, and cultural artifacts. What has been missing, however, is living tissue from some of our lost ancestors and from our closest relatives, like chimps and bonobos.

We have established a bank of cellular tissues from many of our closest relatives that allows us to look at distinctions between ourselves and our closest relatives. As Pascal mentioned, chimpanzees and bonobos are our closest relatives, with 95 percent of our genomes being similar; yet, there are vast differences in phenotype.

How can we begin to understand the cellular and molecular mechanisms responsible for these differences? One of the things we can do is take somatic cells, such as blood cells or skin cells, from all of our closest relatives. Through a process called reprogramming — by overexpression of certain genes in these cells — we can turn the skin or somatic cell into a primitive cell, called an induced pluripotent stem iPS cell. These primitive cells are in a proliferating, living state that can be differentiated to form, in a dish, any cell of the body, allowing us, for the first time, to form living neurons or living heart cells from all of our closest relatives and then compare them across species.

These iPS cells represent a primitive state of development prior to the germ cell. So any change detected in these iPS cells will be passed along to their progeny through the germ cell and into their living progeny. Now a little bit of a disclaimer for those of us who work in this field: these cells have limitations. They are cells in culture. We cannot really look at social experience, and their relevance to a living organism is oftentimes questionable. But we can ask the question: are there differences that are detectable at a cellular and molecular level that help us understand the origin of humans?

We have begun building a library with other collaborators around the world, and have reprogrammed somatic cells from many of these species into iPS cells. They retain common features of embryonic stem cells at the cellular level and they have the same genetic makeup as predicted based on the species.

In our first attempt to see if we could identify differences in these primitive cells, we did what is called a complete transcriptional mRNA analysis. If we compare the transcriptional genomes of chimpanzees and bonobos, there are very few differences. So we pooled all our animals together and compared that combined nonhuman primate group to the human group. In analyzing these genomes, we detected two very interesting genes. Why are we interested in these two proteins?

These two proteins are active suppressors of the activity of what we call mobile elements, which are genetic elements that exist in all of our genomes.

In fact, 50 percent of the DNA in human genomes is made up of these mobile elements molecular parasites of the genome.

So what are mobile elements? They are elements that exist in specific locations in the genome and, through unique mechanisms, they can make copies of themselves and jump from one part of the genome to another. Barbara McClintock discovered these elements through her work on maize.

Some of us study a specific form of mobile elements called a LINE-1 retrotransposon. They exist in thousands of copies in the genome, as a DNA that makes a strand of RNA and then makes proteins that binds back onto the RNA, helping the element copy itself. This combination of mRNA and proteins then moves back into the nucleus where the DNA resides and pastes itself into the genome at a new location.

These LINE elements continue to be active in our genome, and they are particularly active in neural progenitor cells. Not only do humans make more of these proteins, but as an apparent consequence, the lower levels of these L1 suppressors in chimpanzees and bonobos means the L1 elements are much more active in chimpanzees and bonobos than in humans.

When searching the DNA libraries genomes that have been sequenced for chimps, bonobos, and humans, there are many more L1 DNA elements in the genomes of chimps and bonobos relative to humans. This greater number of L1 elements in non-human primate genomes leads to an increase in DNA diversity and, thus, in the diversity of their offspring and potentially in their behavior.

This led us to speculate that this decrease in genetic diversity that occurs in humans leads to a greater dependence on cultural adaptive changes to survive as a species rather than genetic adaptive changes.

For example, if a virus were to infect a chimp or a bonobo population, in order for that species to survive it would require a member of the species with the genetic mutation that provided protection in some form from the virus.

Humans do not wait for the mutation from a member of the species that would provide protection from the virus. We build hospitals, we design antibodies, we transmit our knowledge through cultural information cultural evolution rather than relying on genetics genetic evolution for the spread and the survival of the species. I n the s, my research group happened to discover the first known genetic difference between humans and chimpanzees.

And so I thought, well, they must be just like us. And, indeed, when I first looked at the major causes of death in adult captive chimpanzees, the number one killer was heart disease, heart attacks, and heart failure. Again, I thought, well, they are just like humans. But then when I started going over the textbook with the veterinarian, I noticed that not all the diseases were the same.

So the question arises: are there human-specific diseases? There are a few criteria for human-specific diseases: they are very common in humans but rarely reported in great apes, even in captivity; and they cannot be experimentally reproduced in apes in the days when such studies were allowed.

The caveat, of course, is that reliable information is limited to data on a few thousand Great Apes in captivity. But these apes were cared for in NIH-funded facilities with full veterinary care — probably better medical care than most Americans get — and there were thorough necropsies. As it turned out, I was even wrong about heart disease. It was not until my spouse and collaborator Nissi Varki looked at the pathology that she realized that while heart disease is common in both humans and chimpanzees, it is caused by different pathological processes.

They developed massive scar tissue replacing their heart muscle, which is called interstitial myocardial fibrosis. There is now a special project called The Great Ape Heart Project, which is providing clinical, pathologic, and research strategies to aid in the understanding and treatment of cardiac disease in all of the ape species. There are actually two mysteries to be solved: why do humans not often suffer from the fibrotic heart disease that is so common in our closest evolutionary cousins?

Conversely, why do the Great Apes not often have the kind of heart disease that is common in humans? We put together a list of candidates of human-specific diseases that meet the criteria I mentioned earlier, and myocardial infarction is number one. Spinozzi, G. Local advantage in the visual processing of hierarchical stimuli following manipulations of stimulus size and element numerosity in monkeys Cebus apella. Behav Brain Res. Fagot, J. Global and local processing in humans Homo sapiens and chimpanzees Pan troglodytes : use of a visual search task with com- pound stimuli.

Global and local visual processing by chimpanzees Pan troglodytes. Jpn J Psychon Sci. Google Scholar. Cook, R. Avian detection and identification of perceptual organization in random noise. Behav Process. Nakamura, N. Pigeons perceive the Ebbinghaus-Titchener circles as an assimilation illusion. Watanabe, S. Cognit , — Fujita, K. Better living by not completing: a wonderful peculiarity of pigeon vision?

Behav Processes 69, 59—66 Ushitani, T. Tanaka, H. Global and local processing of visual patterns in macaque monkeys. Neuroreport 11, — Neiworth, J. Global and local processing in adult humans Homo sapiens , 5-year-oldchildren Homo sapiens and adult cotton-top tamarins Saguinus oedipus. J Comp Psychol. Colombo, J. Individual differences in infant visual attention: Are short lookers faster processors or feature processors? Child Dev 62, — Frick, J.

Temporal sequence of global — local processing in 3-month-old infants. Infancy 1, — Freeseman, L. Individual differences in infant visual attention: Four-month-olds' discrimination and generalization of global and local stimulus properties.

Child Development 64, — Guy, M. Visual attention to global and local stimulus properties in 6-month-old infants: Individual differences and event-related potentials.

Child development, Mondloch, C. Developmental changes in the processing of hierarchical shapes continue into adolescence. Experimental Child Psychology 84, 20—40 Helmholtz, H.

Handbook of physiological optics: JS Southhall translation 3 rd ed. Parks, T. Post-retinal visual storage. Zollner, F. Uber eine neue Art anorthoscopischer Zerrbilder. Annalen der Physik und Chemie: Poggendorffs Annalen , — Non-retinotopic feature processing in the absence of retinotopic spatial layout and the construction of perceptual space from motion. Vision Research 71, 10—17 Nakano, T. Deficit in visual temporal integration in autism spectrum disorders. Yin, C. Dynamic shape integration in extrastriate cortex.

Visual search for moving and stationary items in chimpanzees Pan troglodytes and humans Homo sapiens. Atten Percept Psychophys.

Imura, T. Moving shadows contribute to the corridor illusion in a chimpanzee Pan troglodytes. Journal of Comparative Psychology , — Ferber, S. The lateral occipital complex subserves the perceptual persistence of motion-defined groupings. Cereb Cortex 7, — Orban, G. Similarities and differences in motion processing between the human and macaque brain: evidence from fMRI. Neuropsychologia 41, — Comparative mapping of higher visual areas in monkeys and humans.

Trends Cogn. Vanduffel, W. Extracting 3D from motion: differences in human and monkey intraparietal cortex. Science , — The effects of linear perspective on relative size discrimination in chimpanzees Pan troglodytes and humans Homo sapiens. Behav Processes 77, — Matsuzawa, T. The Ai project: historical and ecological contexts.

Animal Cognition 6, — Matsuzawa T. Cognitive development in chimpanzees. Tokyo: Springer-Verlag Tokyo Snodgrass, J. Totally, about human-specific neuronal enhancers were identified, and one of them located on the 8q It was assumed by the authors that recent human-specific enhancers, adaptive, on the one hand, may also impact age-related diseases [ 52 ].

It has been postulated few decades ago that differences between humans and chimpanzees are mostly caused by gene regulation changes rather than by alterations in their protein-coding sequences, and that these changes must affect embryo development [ 6 ]. For example, evolutional acquisitions such as enlarged brain or modified arm emerged as a result of developmental changes during embryogenesis [ , ].

Such changes include when, where and how genes are expressed. A plethora of genes involved in embryogenesis have pleiotropic effects [ ] and mutations within their coding sequence may cause complex, mostly negative, consequences for an organism. On the other hand, changes in gene regulation could be limited to a certain tissue or time frame that can enable fine tuning of a gene activity [ ].

Indeed, the fast-evolving sequences HARs or HACNs are often found close to the genes active during embryo- and neurogenesis [ 48 , 49 , 50 , ].

For example, HACNS1 HAR2 demonstrates greater enhancer activity in limb buds of transgenic mice compared to orthologous sequences from chimpanzee or rhesus macaque [ ]. Many studies were focused on finding differences between humans, chimpanzees and other mammals at the level of gene transcription [ , , ].

Importantly, tissue-specific differences within the same species significantly exceeded in amplitude all species-specific differences in any tissue. The most transcriptionally divergent organs between humans and chimpanzees were liver and testis, and to a lesser extent — kidney and heart [ , ]. A transcriptional distinction of liver may be a consequence of different nutritional adaptations in the two species.

The major differences in testes are largely unexplained but may be related to predominantly monogamous behavior in humans. Surprisingly, the brain was the least divergent organ between humans and chimpanzees at the transcriptional level. In this regard, it is suggested that tighter regulation of signaling pathways in the brain underlies behavioral and cognitive differences [ , ]. However, it was found that during evolution in the human cerebral cortex there were more transcriptional changes than in the chimpanzee [ ].

Among them, the prevailed difference was increased transcriptional activity [ , ]. Another study of transcriptional activity in the forebrain evidenced the higher difference between human and chimpanzee in the frontal lobe [ ]. The functions of frontal lobe-specific groups of co-expressed genes dealt mostly with neurogenesis and cell adhesion [ ]. Furthermore, the analysis of genes associated with communication showed that about a quarter of them was differentially expressed in the brains of humans and other primates [ ].

Remarkably, the KRAB-ZNF gene family is known for its rapid evolution in primates, especially for its human- or chimpanzee-specific members [ ]. The studies of transcriptional timing in the postnatal brain development also revealed a number of human-specific features. A specific set of genes was found whose expression was delayed in humans compared to the other primates. It is congruent with the prolonged brain development period in humans relative to other primates [ , ].

The results recently published by Pollen and colleagues allowed to look deeper into the developing human and chimpanzee brains by applying the organoid model [ ]. Cerebral organoids were generated from induced pluripotent stem cells iPSCs of humans and chimpanzees.

Transcriptome analyses revealed genes deferentially expressed in human versus chimpanzee cerebral organoids and macaque cortex. Epigenetic regulation is another factor that should be considered when looking at interspecies differences in gene expression. High throughput analysis of differentially methylated DNA in human and chimpanzee brains showed that human promoters had lower degree of methylation. The analysis of H3K4me3 trimethylated histone H3 is a marker of transcriptionally active chromatin distribution in the neurons of prefrontal lobe revealed human-specific regions, 33 of them were neuron-specific.

Another active chromatin biomarker is the distribution of DNase I hypersensitivity sites DHSs , that often indicate gene regulatory elements. Using chromatin immunoprecipitation assay, a number of haDHSs interacting genes were identified, many of which were connected with early development and neurogenesis [ 3 , ].

In a later study [ ], about 3,5 thousand haDHSs were found, that were enriched near the genes related to neuronal functioning [ ]. It is now generally accepted that both changes in gene regulation and alterations of protein coding sequences might have played a major role in shaping the phenotypic differences between humans and chimpanzees.

In this context, complex bioinformatic approaches combining various OMICS data analyses, are becoming the key for finding genetic elements that contributed to human evolution. It is also extremely important to have relevant experimental models to validate the candidate species-specific genomic alterations.

However, at least for now using these experimental approaches for millions of species specific potentially impactful features reviewed here is impossible due to high costs and labor intensity. In turn, an alternative approach could be combining the refined data in a realistic model of human-specific development using a new generation systems biology approach trained on a functional genomic Big Data of humans and other primates.

Such an approach could integrate knowledge of protein-protein interactions, biochemical pathways, spatio-temporal epigenetic, transcriptomic and proteomic patterns as well as high throughput simulation of functional changes caused by altered protein structures. The differences revealed could be also analyzed in the context of mammalian and primate-specific evolutionary trends, e. Apart from the single-gene level of data analysis, this information could be aggregated to look at the whole organismic, developmental or intracellular processes e.

And finally, most of the results described here were obtained for the human and chimpanzee reference genomes, which were built each using DNAs of several individuals. Nowadays the greater availability of whole-genome sequencing highlighted the next challenge in human and chimpanzee comparison — populational genome diversity.

For example, the recent study [ ] of native African genomes was focused on the fraction of sequences absent from the reference Hg38 genome assembly. Furthermore, it also reflects the high degree of genome heterogeneity of the African population [ ]. Similar studies were performed for other populations as well. The chimpanzees also demonstrate substantial genome diversity with many population-specific traits: the central chimpanzees retain the highest diversity in the chimpanzee lineage, whereas the other subspecies show multiple signs of population bottlenecks [ ].

So far there were not so many studies published on the topic of non-reference human and chimpanzee genome comparison. However, some estimates can be made. As expected, NSs were enriched in simple repeats and satellites and varied greatly among the individuals. The most part of NSs 32, aligned confidently to the non-reference sequences from the aforementioned study of African genomes [ ].

Finally, as many as 18, NSs were present also in the chimpanzee PT4 genome assembly. Positioning of NS insertions in the human genome revealed that of them located within genes, where 85 NS insertion events were found within the exons of 82 genes [ ].

Another research consortium studied non-repetitive non-reference sequences NRNR in the genomes of 15, Icelanders [ ]. Thus, the lack of information on genome populational diversity could impact the total extent of human and chimpanzee interspecies divergence by misinterpretation of polymorphic sequences. Still, these findings inevitably lead to the idea of the need, firstly, to create, and secondly, to compare human and chimpanzee pan-genomes. Amster G, Sella G. Life history effects on the molecular clock of autosomes and sex chromosomes.

Langergraber KE, et al. Generation times in wild chimpanzees and gorillas suggest earlier divergence times in great ape and human evolution. Lu Y, et al. Evolution and comprehensive analysis of DNaseI hypersensitive sites in regulatory regions of primate brain-related genes.

Front Genet. Bauernfeind AL, et al. High spatial resolution proteomic comparison of the brain in humans and chimpanzees. J Comp Neurol. Prescott SL, et al. Enhancer divergence and cis-regulatory evolution in the human and chimp neural crest. Evolution at two levels in humans and chimpanzees. Lander ES, et al. Initial sequencing and analysis of the human genome. Initial sequence of the chimpanzee genome and comparison with the human genome. Google Scholar. The striking resemblance of high-resolution G-banded chromosomes of man and chimpanzee.

Szamalek JM, et al. The chimpanzee-specific pericentric inversions that distinguish humans and chimpanzees have identical breakpoints in Pan troglodytes and Pan paniscus. Goidts V, et al. Independent intrachromosomal recombination events underlie the pericentric inversions of chimpanzee and gorilla chromosomes homologous to human chromosome Genome Res. Kehrer-Sawatzki H, et al. Molecular characterization of the pericentric inversion that causes differences between chimpanzee chromosome 19 and human chromosome Am J Hum Genet.

Flaquer A, et al. The human pseudoautosomal regions: a review for genetic epidemiologists. Eur J Hum Genet. Ross MT, et al. The DNA sequence of the human X chromosome. Funct Integr Genomics. Balasubramanian S, et al. Comparative analysis of processed ribosomal protein pseudogenes in four mammalian genomes. Genome Biol. Fortna A, et al. Lineage-specific gene duplication and loss in human and great ape evolution. PLoS Biol. Charrier C, et al. Inhibition of SRGAP2 function by its human-specific paralogs induces neoteny during spine maturation.

McLean CY, et al. Human-specific loss of regulatory DNA and the evolution of human-specific traits. Hayakawa T, et al. Alu-mediated inactivation of the human CMP- N-acetylneuraminic acid hydroxylase gene. Sen SK, et al.

Human genomic deletions mediated by recombination between Alu elements. Han K, et al. L1 recombination-associated deletions generate human genomic variation. Genomic rearrangements by LINE-1 insertion-mediated deletion in the human and chimpanzee lineages. Nucleic Acids Res. Lee J, et al. Human genomic deletions generated by SVA-associated events.

Comp Funct Genomics. Alu recombination-mediated structural deletions in the chimpanzee genome. PLoS Genet. Mills RE, et al. Recently mobilized transposons in the human and chimpanzee genomes. Tang W, et al. Mobile elements contribute to the uniqueness of human genome with 15, human-specific insertions and 14 Mbp sequence increase.

DNA Res. Different evolutionary fates of recently integrated human and chimpanzee LINE-1 retrotransposons. Biochemistry Mosc. CAS Google Scholar. Zabolotneva AA, et al. Medstrand P, Mager DL. J Virol. Buzdin A, et al. A technique for genome-wide identification of differences in the interspersed repeats integrations between closely related genomes and its application to detection of human-specific integrations of HERV-K LTRs. Genome-wide experimental identification and functional analysis of human specific retroelements.

Cytogenet Genome Res. Mamedov I, et al. Genome-wide comparison of differences in the integration sites of interspersed repeats between closely related genomes. Contreras-Galindo R, et al. HIV infection reveals widespread expansion of novel centromeric human endogenous retroviruses. Zahn J, et al. Expansion of a novel endogenous retrovirus throughout the pericentromeres of modern humans. Chimpanzee S, Analysis C. Genome-wide amplification of proviral sequences reveals new polymorphic HERV-K HML-2 proviruses in humans and chimpanzees that are absent from genome assemblies.

Mun S, et al. Chimpanzee-specific endogenous retrovirus generates genomic variations in the chimpanzee genome. PLoS One. Go Y, Niimura Y. Similar numbers but different repertoires of olfactory receptor genes in humans and chimpanzees.

Mol Biol Evol. Zhang XM, et al. The human T-cell receptor gamma variable pseudogene V10 is a distinctive marker of human speciation. Winter H, et al. Human type I hair keratin pseudogene phihHaA has functional orthologs in the chimpanzee and gorilla: evidence for recent inactivation of the human gene after the Pan-Homo divergence. Hum Genet. Enard W, et al. Molecular evolution of FOXP2, a gene involved in speech and language.

Accelerated protein evolution and origins of human-specific features: Foxp2 as an example. Schreiweis C, et al. Humanized Foxp2 accelerates learning by enhancing transitions from declarative to procedural performance.

Evans PD, et al. Microcephalin, a gene regulating brain size, continues to evolve adaptively in humans. Adaptive evolution of ASPM, a major determinant of cerebral cortical size in humans. Hum Mol Genet. Pollard KS, et al. An RNA gene expressed during cortical development evolved rapidly in humans. Prabhakar S, et al.

Accelerated evolution of conserved noncoding sequences in humans.