Aquatic Ape Human Ancestor Theory

Aquatic Ape Theory - What is it?

A Brief Summary of AAT - key arguments

A Brief History and Key Proponents of AAT

When / Where / How?

Ape to Human Evolution Timeline

Alternative theories of human evolution

Wikipedia and the scientific community

... Anatomical Evidence
... Bipedalism
... Birth and babies
... Brain
... Breath control
... Descended larynx
... Diet
... Diseases
... Fat
... Fingers, toes and feet
... Furlessness
... Hair and baldness
... Human ailments
... Kidneys
... Language & Song
... Menopause
... Nose
... Olfactory sense
... Pachyostosis
... Paranasal Sinuses
... Platycephaly
... Reverse osmosis
... Sexual features
... Sleep (USWS)
... Surfer's ear
... Sweating
... Tears
... Underwater vision
... Viruses
... Waterside environments

. Homo Ancestors
... Trachillos bipedal hominids
... Homo erectus
... Homo neanderthalensis
... Sea Gypsies/ the Moken
... Homo sapiens - water afinity
... Coastal Migration
... Pan and Gorilla ancestry
... Semi-Aquatic Animals

. Testable Hypotheses
. Fossil evidence
. Genetic evidence
. Paleoecological evidence
. Retroviral marker in apes
. Acheulean handaxes

A call to scientists...

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Genetic Evidence

A new gene has been identified in humans that is not present in other apes, shedding more light on human evolution. Researchers of the University of Edinburgh (UK) compared the human genome to 11 other mammalian species, including chimps, gorillas, mice and rats. They found that only humans possessed the gene miR-941. This is a stark contrast to previous genetic differences found between us and our ape cousins, which indicated changes to genes rather than totally new ones (a good example of this is the FoxP2 gene - though we have different versions with different
effects, we still both have the gene). Further testing revealed that this gene is highly active in two brain areas that make humans so successful - tool use and language abilities.

These results strongly indicate that miR-941 makes a large contribution to our higher brain functions. The fact that only we have this gene is remarkable. Differences between species are usually a result of changes to genes, duplication or deletion. But miR-941 seems to have emerged fully-
functional out of "junk" DNA (non-coding genetic material), and its emergence was extremely brief in evolutionary terms. It's also estimated this gene emerged between 1 and 6 million years ago, after humans and chimps had split from their last common ancestor. Dr. Martin Taylor, who led the study, commented, "As a species, humans are wonderfully inventive -- we are socially and technologically evolving all the time. But this research shows
that we are innovating at a genetic level too. This new molecule sprang from nowhere at a time when our species was undergoing dramatic changes: living longer, walking upright, learning how to use tools and how to communicate. We're now hopeful that we will find more new genes that help show what makes us human."

http://www.sciencedaily.com/releases/2012/11/121114113458.htm
http://www.medicalnewstoday.com/articles/252822.php
http://www.nature.com/ncomms/journal/v3/n10/full/ncomms2146.html

Why Can't Chimps Speak? Key Differences In How Human And Chimp Versions Of FOXP2 Gene Work

Date: November 12, 2009
Source: University of California - Los Angeles
Summary: If humans are genetically related to chimps, why did our brains develop the innate ability for language and speech while theirs did not? Scientists suspect that part of the answer to the mystery lies in a gene called FOXP2. When mutated, FOXP2 can disrupt speech and language in humans. Now, a new study reveals major differences between how the human and chimp versions of FOXP2 work, perhaps explaining why language is unique to humans.

If humans are genetically related to chimps, why did our brains develop the innate ability for language and speech while theirs did not?

Scientists suspect that part of the answer to the mystery lies in a gene called FOXP2. When mutated, FOXP2 can disrupt speech and language in humans. Now, a UCLA/Emory study reveals major differences between how the human and chimp versions of FOXP2 work, perhaps explaining why language is unique to humans.

Published Nov. 11 in the sonline edition of the journal Nature, the findings provide insight into the evolution of the human brain and may point to possible drug targets for human disorders characterized by speech disruption, such as autism and schizophrenia.

"Earlier research suggests that the amino-acid composition of human FOXP2 changed rapidly around the same time that language emerged in modern humans," said Dr. Daniel Geschwind, Gordon and Virginia MacDonald Distinguished Chair in Human Genetics at the David Geffen School of Medicine at UCLA. "Ours is the first study to examine the effect of these amino-acid substitutions in FOXP2 in human cells.

"We showed that the human and chimp versions of FOXP2 not only look different but function differently too," said Geschwind, who is currently a visiting professor at the Institute of Psychiatry at King's College London. "Our findings may shed light on why human brains are born with the circuitry for speech and language and chimp brains are not."

FOXP2 switches other genes on and off. Geschwind's lab scoured the genome to determine which genes are targeted by human FOXP2. The team used a combination of human cells, human tissue and post-mortem brain tissue from chimps that died of natural causes.

The chimp brain dissections were performed in the laboratory of coauthor Todd Preuss, associate research professor of neuroscience at Emory University's Yerkes National Primate Research Center.

The scientists focused on gene expression -- the process by which a gene's DNA sequence is converted into cellular proteins.

To their surprise, the researchers discovered that the human and chimp forms of FOXP2 produce different effects on gene targets in the human cell lines.

"We found that a significant number of the newly identified targets are expressed differently in human and chimpanzee brains," Geschwind said. "This suggests that FOXP2 drives these genes to behave differently in the two species."

The research demonstrates that mutations believed to be important to FOXP2's evolution in humans change how the gene functions, resulting in different gene targets being switched on or off in human and chimp brains.

"Genetic changes between the human and chimp species hold the clues for how our brains developed their capacity for language," said first author Genevieve Konopka, a postdoctoral fellow in neurology at the David Geffen School of Medicine at UCLA. "By pinpointing the genes influenced by FOXP2, we have identified a new set of tools for studying how human speech could be regulated at the molecular level."

The discovery will provide insight into the evolution of humans' ability to learn through the use of higher cognitive skills, such as perception, intuition and reasoning.

"This study demonstrates how critical chimps and macaques are for studying humans," noted Preuss. "They open a window into understanding how we evolved into who we are today."

Because speech problems are common to both autism and schizophrenia, the new molecular pathways will also shed light on how these disorders disturb the brain's ability to process language.

The National Institute of Mental Health, the A.P. Giannini Foundation and the National Alliance for Research on Schizophrenia and Depression funded the study.

The UCLA coauthors included Jamee Bomar, Giovanni Coppola, Fuying Gao, Zophonias Jonsson, Sophia Peng, Kellen Winden and James Wohlschlegel.


http://www.sciencedaily.com/releases/2009/11/091111130942.htm


 
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