Affichage des articles dont le libellé est Évolution humaine. Afficher tous les articles
Affichage des articles dont le libellé est Évolution humaine. Afficher tous les articles
Nous rions depuis 15 millions d'années
We share 98.9 percent percent of our DNA with many of our primate cousins, but we also may share something a little more silly. Modern humans and great apes may have been laughing for at least 15 million years. The findings, published today in the journal Communications Biology, shed new light on how our speech evolved.
“How did humans evolve the remarkable ability to speak? Speech leaves no fossils, and complex language exists only in our own species,” Dr. Chiara De Gregorio, a study co-author and primatologist at the University of Warwick, said in a statement. “But we’ve found a 15-million-year-old clue in an unexpected place: our laughter.”
All living great apes (orangutans, bonobos, chimpanzees, gorillas, and humans) laugh. However, it’s been unclear how laughter may have changed the past several million years of evolution and how it may relate to human speech evolution.
In this new study, a team from the University of Warwick in the United Kingdom analyzed recordings from four orangutans, two gorillas, four chimpanzees, three bonobos, two gorillas, and four humans. They found the same pattern across 14 laughter sequences—all six species laugh with evenly spaced rhythmic intervals between successive sounds.
According to the team, this basic rhythmic structure was likely already present in a shared common ancestor 15 million years ago. This structure has also remained with all living great apes over all that time, since all great apes show the same underlying speech pattern.
“By comparing how different species laugh, we can see that a basic rhythmic structure has remained unchanged since our last common ancestor,” De Gregorio said. “That’s extraordinary.”
While the basic rhythm has stayed constant, human laughter has changed a bit. It’s become faster, more variable, and gained sophisticated control that is dependent on the context. Humans are the only great apes that have this ability to (mostly) control when and how they laugh depending on the situation. An uncontrollable laugh when tickled is vastly different from a polite laugh in a meeting, an infectious laugh during a movie, or a nervous little giggle after making a mistake. That same underlying rhythm in laughter is shaped by a conscious control to communicate varying emotions and intentions.
These findings suggest that throughout great ape evolution, our ancestors gradually developed more control over the timing of their vocalizations, including laughter. Scientists consider sophisticated vocal control like this as a fundamental building block of speech.
Since laughter has such deep evolutionary roots and has remained shared by all living great apes for millennia, it is one of the easiest ways to study how the vocal transformations changed across hominid evolution.
“Contrary to the classic notion that the first humans suddenly acquired vocal control capacities remarkably different from their predecessors, laughter evolution tells us that humans lay on a continuum, a prolongation of vocal control capacities that were already being cumulatively honed in for 15 million years,” study co-author and primatologist Dr. Adriano Lameria concluded.
Les Européens ont beaucoup évolué au cours des derniers millénaires
A massive study of ancient DNA from nearly 16,000 people across more than 10,000 years in West Eurasia reveals that natural selection has shaped modern human genomes far more than previously thought.
Before now, studies of ancient human DNA had identified only about 21 instances of directional selection — the type of natural selection that occurs when one version of a gene that confers an extreme form of a trait, such as lactose tolerance after infancy, proves advantageous enough for survival and reproduction that it gets passed on to more offspring than less advantageous versions of the gene and rapidly rises in frequency across a population. The dearth of evidence suggested that directional selection has been rare since modern humans arose in Africa some 300,000 years ago and began to split into different population groups around the world.
Combining an unprecedented amount of ancient genomic data with novel computational methods, the new analysis shows instead that directional selection has driven the spread or decline of hundreds of gene variants in West Eurasia since the end of the Ice Age and that selection has actually accelerated since people transitioned from hunting and gathering to farming.
The work demonstrates the power of ancient-DNA research to illuminate human genetic adaptation and other fundamental principles of evolutionary biology.
Many of the identified gene variants have known links to complex physical, psychological, and social traits, including risk for type 2 diabetes and schizophrenia. Delving into the evolution of these traits could deepen understanding of behavior, health, and disease and inform treatment efforts. However, the way we define some of the traits today, such as household income, doesn’t translate to prehistoric contexts, and the current analysis can’t speak to what made a variant beneficial for survival when it first arose.
The findings, led by Harvard University researchers, are published April 15 in Nature.
“With these new techniques and large amount of ancient genomic data, we can now watch how selection shaped biology in real time,” said Ali Akbari, first author of the study and senior staff scientist in the lab of Harvard geneticist David Reich. “Instead of searching for the scars natural selection leaves in present-day genomes using simple models and assumptions, we can let the data speak for itself.”
“This work allows us to assign place and time to forces that shaped us,” said Reich, professor of genetics in the Blavatnik Institute at Harvard Medical School, professor of human evolutionary biology in the Harvard University Faculty of Arts and Sciences, and senior author of the study.
10,000 ancient genomes, new computational methods
Since 2010, when the first genome-wide data was recovered from ancient human remains, ancient-DNA research has expanded understanding of the relationships among people living in different time periods and regions of the world.
But geneticists struggled to realize the technology’s promise to illuminate how natural selection has shaped human genetic variation even over the last 10,000 years, when there is enough well-preserved genetic material to support large-scale studies.
The new study broke through that barrier using two innovations.
First, the Reich Lab spent seven years building a collection of DNA sequences from ancient people living in West Eurasia — what is now Europe and parts of the Middle East — that would be comprehensive enough in size and time span to support the work.
“If the goal is to uncover changes in the frequency of genetic variants in the last ten millennia that are greater than can be expected by chance, then we need to detect subtle effects, which requires having thousands of genomes spanning that time period,” explained Reich, who is also a member of the Broad Institute of MIT and Harvard and a Howard Hughes Medical Institute Investigator.
The lab collaborated with more than 250 archeologists and anthropologists to report new DNA data from 10,016 ancient individuals from West Eurasia. They added those to another 5,820 published ancient sequences and 6,438 modern ones.
“This single paper doubles the size of the ancient human DNA literature,” Reich said. “It reflects a focused effort to fill in holes that limited the power of previous studies to detect selection.”
The second innovation — and even more important to the success of the study, Reich said — was Akbari’s development of computational methods to isolate the signal of directional selection from other causes of gene frequency changes, such as human migration, population mixing, and random genetic fluctuations that occur in small populations.
“Ali developed a powerful technique that could zoom in on the patterns that actually mattered,” said Reich.
In the end, it was a faint signal indeed that Akbari detected. By the team’s calculations, directional selection accounted for only about 2 percent of all gene frequency changes.
What has natural selection selected for?
Two percent still encompasses a lot of DNA. Akbari identified 479 gene versions, or alleles, that were strongly selected for — or against — in West Eurasian genomes.
He and colleagues were able to ascertain when and where some of the alleles began to spread through or be pushed out of the West Eurasian gene pool. They also calculated an overall rate at which selection seemed to occur and detected changes in that rate. They found that selection accelerated after the introduction of farming, reflecting how different traits became advantageous as people shifted to agricultural environments and behaviors.
More than 60 percent of the individual DNA variants that were flagged as being strongly selected for — most of them single nucleotide polymorphisms, or SNPs — have documented links with present-day human traits, such as:
-Light skin tone
-Red hair
-Risk of celiac disease and Crohn’s disease
-Immunity to HIV infection and resistance to leprosy
-Lower chance of male-pattern baldness
-Lower risk of rheumatoid arthritis and alcoholism
-Having the B version of the proteins on red blood cells that confer A, B, and O blood types and influence resistance to infection with bacteria and viruses
In some cases, groups of SNPs were under selection together to influence polygenic traits. Some changes raised the frequency of beneficial traits, including some that are interpreted today as:
-“Health span” traits such as faster walking pace
-Measures of behavioral and social status or cognitive functions, such as scores on intelligence tests, household income, and years of schooling
Other changes reduced the frequency of harmful traits, such as those that are interpreted today as:
-Reduced risk of bipolar disorder and schizophrenia
-Lower body fat percentage, waist-to-hip ratio, and body mass index
-Less susceptibility to tobacco smoking
Still other SNPs, such as some that today are associated with susceptibility to tuberculosis and multiple sclerosis, at first rose and then fell in frequency over the millennia, indicating shifts in environmental pressures and the traits that prove beneficial, the team found.
Some of the links seem logical, others counterintuitive, like the major genetic risk factor for gluten intolerance spiking after people began farming wheat.
However, the authors emphasize that there are several crucial factors to understand before interpreting SNP associations like these.
First: What a variant is associated with now is not necessarily why an allele propagated in the West Eurasian gene pool. Reasons for this include:
-Some of the traits that SNPs are associated with in modern societies did not exist in ancient contexts and therefore can’t explain why an allele was originally advantageous or detrimental. A variant that now correlates to household income or years of schooling had to have meant something different in the Stone Age. So these results do not mean that Europeans evolved to be smarter or healthier.
-The fact that an allele shapes a particular trait today also does not automatically mean this trait was important in the past. Perhaps having red hair was beneficial 4,000 years ago, or perhaps it came along for the ride with a more important trait.
-Some SNPs affect multiple traits, so what a genomic database tags a SNP as affecting may not capture everything it’s doing. Today, for instance, we know that the same gene variant that raises risk of sickle cell disease also protects people from malaria, so what looks like natural selection for one disease may be selection against another.
-It’s possible that a flagged SNP is actually in a gene next to the one that natural selection was targeting — another way of coming along for the ride.
-Present-day traits a SNP influences may not yet be known or included in the databases the team analyzed.
Second: Just because an allele, SNP, or trait swept into or out of West Eurasia during this time doesn’t mean this happened only in West Eurasia. Researchers can use the new computational methods to look for directional selection in other populations worldwide that have enough ancient DNA sequences and construct a clearer picture of what’s unique to different groups and what generalizes across populations.
Reich expects that future studies will show that shared selective pressures acted on some of the same core traits across diverse human groups, even as those groups split off and migrated to different parts of the world over tens of thousands of years.
Le sinus préauriculaire
Ces gens qui vivent avec des branchies !
Certaines personnes naissent avec une malformation (bénigne) du premier et deuxième arcs pharyngés qui fait apparaitre un petit trou, le sinus préauriculaire, à l'avant des oreilles.
Ce trou est l'équivalent du spiracle des requins, qui est lui-même la relique évolutive des deux mêmes arcs branchiaux. Chez les poissons à machoîre (nos ancêtres inclus), les arcs qui soutenaient la première et seconde paires de branchies sont en effet devenus la mandibule, et le spiracle représente ce qui reste de leur ouverture extérieure.
Le sinus préauriculaire est donc le témoin direct de notre origine parmi les animaux que nous appelons poisson !
Encore une belle preuve de l'évolution.
En savoir plus: https://www.youtube.com/watch?v=GD3Yft_saZ8
The emergence of genetic variants linked to brain and cognitive traits in human evolution (Ilan Libedinsky)
Human evolution involved major anatomical transformations, including a rapid increase in brain volume over the last 2 million years. Examination of fossil records provides insight into these physical changes but offers limited information on the evolution of brain function and cognition.
A complementary approach integrates genome dating from the Human Genome Dating Project with genome-wide association studies to trace the emergence of genetic variants linked to human traits over 5 million years. We find that genetic variants underlying cortical morphology (~300,000 years, P = 4 × 10-28), fluid intelligence (~500,000 years, P = 1.4 × 10-4), and psychiatric disorders (~475,000 years, P = 5.9 × 10-33) emerged relatively recently in hominin evolution. Among psychiatric phenotypes, variants associated with depression (~24,000 years, P = 1.6 × 10-4) and alcoholism-related traits (~40,000 years, P = 5.2 × 10-12) are the youngest.
Genes with recent evolutionary modifications are involved in intelligence (P = 1.7 × 10-6) and cortical area (P = 3.5 × 10-4) and exhibit elevated expression in language-related areas (P = 7.1 × 10-4), a hallmark of human cognition. Our findings suggest that recently evolved genetic variants shaped the human brain, cognition, and psychiatric traits.
Vos cellules immunitaires sculptent votre intelligence avant même votre naissance – et ça ne marche que chez les humains !
Une équipe de scientifiques vient de faire une découverte qui pourrait révolutionner notre compréhension de l’évolution humaine et expliquer pourquoi notre cerveau est si différent de celui des autres espèces. En étudiant le développement cérébral dans l’utérus, les chercheurs ont en effet révélé que nos cellules immunitaires jouent un rôle totalement inattendu : elles orchestrent littéralement la construction de notre intelligence. Cette trouvaille, publiée dans la prestigieuse revue Nature, pourrait non seulement éclairer les origines de nos capacités cognitives exceptionnelles, mais aussi ouvrir de nouvelles pistes pour comprendre des troubles comme l’autisme, l’épilepsie et la schizophrénie.
Le cerveau humain : une architecture unique au monde
Pour saisir l’importance de cette découverte, il faut d’abord comprendre ce qui rend notre cerveau si particulier. Le cortex humain, cette couche ridée qui recouvre la surface de notre cerveau, abrite une population neuronale d’une richesse extraordinaire. Parmi ces milliards de cellules nerveuses, un type particulier attire aujourd’hui toute l’attention des neuroscientifiques : les interneurones inhibiteurs.
Ces cellules représentent entre 25 et 50% de tous les neurones corticaux chez l’adulte, une proportion remarquable qui dépasse largement celle observée chez nos cousins mammifères. À titre de comparaison, le cerveau humain contient plus du double d’interneurones par rapport au cerveau de souris. Cette différence quantitative cache une fonction capitale : ces neurones spécialisés régulent l’activité cérébrale grâce à un messager chimique appelé GABA.
Le GABA agit comme un véritable chef d’orchestre neuronal, ralentissant l’activité cérébrale et équilibrant les signaux excitateurs qui tendent à amplifier la communication entre neurones. Sans cette régulation fine, le cerveau sombre dans le chaos : l’épilepsie, l’autisme et la schizophrénie sont d’ailleurs tous associés à des dysfonctionnements de ces interneurones inhibiteurs.
Une découverte née de l’innovation technologique
L’équipe dirigée par Diankun Yu et le Dr Xianhua Piao de l’Université de Californie à San Francisco s’est heurtée à un défi majeur : comment étudier un phénomène qui semble propre à l’espèce humaine ? Les modèles animaux traditionnels, piliers de la recherche biomédicale, se révélaient inadéquats pour comprendre ce mécanisme particulier.
La solution est venue des organoïdes, ces structures tridimensionnelles cultivées en laboratoire à partir de cellules souches humaines. Ces « mini-cerveaux » reproduisent fidèlement certaines phases du développement cérébral fœtal, offrant une fenêtre unique sur les processus biologiques qui se déroulent dans l’utérus maternel.
L’innovation cruciale de cette recherche a consisté à intégrer dans ces organoïdes la microglie, ces cellules immunitaires résidentes du cerveau. Cette prouesse technique a permis d’observer pour la première fois comment le système immunitaire et le système nerveux collaborent pendant le développement cérébral.
L’acteur inattendu du développement neuronal
Les résultats ont révélé un mécanisme d’une élégance surprenante. La microglie, traditionnellement considérée comme la « police » du cerveau chargée de détecter et éliminer les menaces, s’avère également jouer le rôle d’architecte du développement neuronal. Ces cellules immunitaires produisent massivement une substance appelée IGF1 (facteur de croissance analogue à l’insuline 1).
Cette découverte de l’IGF1 comme signal déclencheur transforme complètement notre vision du développement cérébral. Lorsque la microglie libère cette molécule, elle provoque une multiplication spectaculaire des interneurones inhibiteurs, créant littéralement les fondations neurales de notre intelligence future.
L’expérimentation a confirmé ce lien de causalité : quand les chercheurs bloquent la signalisation IGF1, la prolifération des interneurones s’arrête brutalement. Plus fascinant encore, ce mécanisme semble totalement absent chez la souris, suggérant une adaptation évolutionnaire spécifiquement humaine.
Une clé évolutionnaire de l’intelligence humaine
Cette spécificité humaine ouvre des perspectives vertigineuses sur notre évolution cognitive. Les chercheurs proposent que cette collaboration entre microglie et développement neuronal représente une adaptation évolutionnaire répondant aux besoins particuliers du cerveau humain. Notre cortex, plus complexe et plus étendu que celui de nos proches parents primates, nécessiterait cette production massive d’interneurones pour maintenir son équilibre fonctionnel.
Cette hypothèse pourrait expliquer comment notre lignée a développé des capacités cognitives si exceptionnelles : langage complexe, pensée abstraite, créativité artistique, raisonnement mathématique. Toutes ces facultés reposent sur des circuits neuronaux d’une sophistication inégalée dans le règne animal, circuits dont la construction dépendrait de cette orchestration immunitaire unique.
Vers de nouveaux horizons thérapeutiques
Au-delà de son intérêt évolutionnaire, cette découverte ouvre des pistes thérapeutiques prometteuses. Comprendre comment la microglie influence la formation des interneurones pourrait révolutionner notre approche des troubles neurodéveloppementaux. L’autisme, l’épilepsie et la schizophrénie, tous liés à des dysfonctionnements de ces neurones inhibiteurs, pourraient bénéficier de nouvelles stratégies d’intervention précoce.
Les organoïdes, malgré leurs limitations actuelles pour reproduire les stades tardifs du développement, offrent déjà une plateforme exceptionnelle pour tester de nouvelles approches thérapeutiques. Cette technologie pourrait accélérer considérablement la découverte de traitements personnalisés pour ces pathologies dévastatrices.
Vos cellules immunitaires sculptent votre intelligence avant même votre naissance – et ça ne marche que chez les humains !
Une équipe de scientifiques vient de faire une découverte qui pourrait révolutionner notre compréhension de l’évolution humaine et expliquer pourquoi notre cerveau est si différent de celui des autres espèces. En étudiant le développement cérébral dans l’utérus, les chercheurs ont en effet révélé que nos cellules immunitaires jouent un rôle totalement inattendu : elles orchestrent littéralement la construction de notre intelligence. Cette trouvaille, publiée dans la prestigieuse revue Nature, pourrait non seulement éclairer les origines de nos capacités cognitives exceptionnelles, mais aussi ouvrir de nouvelles pistes pour comprendre des troubles comme l’autisme, l’épilepsie et la schizophrénie.
(...) Les résultats ont révélé un mécanisme d’une élégance surprenante. La microglie, traditionnellement considérée comme la « police » du cerveau chargée de détecter et éliminer les menaces, s’avère également jouer le rôle d’architecte du développement neuronal. Ces cellules immunitaires produisent massivement une substance appelée IGF1 (facteur de croissance analogue à l’insuline 1).
Cette découverte de l’IGF1 comme signal déclencheur transforme complètement notre vision du développement cérébral. Lorsque la microglie libère cette molécule, elle provoque une multiplication spectaculaire des interneurones inhibiteurs, créant littéralement les fondations neurales de notre intelligence future.
L’expérimentation a confirmé ce lien de causalité : quand les chercheurs bloquent la signalisation IGF1, la prolifération des interneurones s’arrête brutalement. Plus fascinant encore, ce mécanisme semble totalement absent chez la souris, suggérant une adaptation évolutionnaire spécifiquement humaine.
Cette spécificité humaine ouvre des perspectives vertigineuses sur notre évolution cognitive. Les chercheurs proposent que cette collaboration entre microglie et développement neuronal représente une adaptation évolutionnaire répondant aux besoins particuliers du cerveau humain. Notre cortex, plus complexe et plus étendu que celui de nos proches parents primates, nécessiterait cette production massive d’interneurones pour maintenir son équilibre fonctionnel.
Cette hypothèse pourrait expliquer comment notre lignée a développé des capacités cognitives si exceptionnelles : langage complexe, pensée abstraite, créativité artistique, raisonnement mathématique. Toutes ces facultés reposent sur des circuits neuronaux d’une sophistication inégalée dans le règne animal, circuits dont la construction dépendrait de cette orchestration immunitaire unique.
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