We have plenty of evidence of "complex" organs evolving from simpler organs. Some of this evidence includes looking at the organs from different creatures. Take the eye for example:
All of the above eyes not only show how the eye evolved but are still in existence because we can find organisms today that still have them!
The molecular mechanisms capable of accomplishing this dramatic evolutionary feat remain a complete mystery to the scientists who study it, yet none dare question it as fact.
Wrong. Researchers say they may have found the missing link to this change in a strand of DNA. Specifically, it is a mutation in a gene that controls muscle development. The mutation just may have caused ancestral jaws to become smaller and weaker over time, eventually making room for a bigger, more complex brain.
"Around the lab, we jokingly call this the 'room for thought' mutation," said Dr. Hansell Stedman, an associate professor of surgery at the University of Pennsylvania School of Medicine.
"We're not saying this mutation alone defines us as Homo sapiens, but the timing of the loss of chewing strength with the increase in cranial capacity is very intriguing."
The researchers are among hundreds around the globe making comparisons between the human gene map and those of other animals, particularly chimpanzees. The Penn scientists' discovery, described Thursday in the journal Nature, grew out of research into the genetic roots for muscular dystrophy, a muscle-wasting disease.
Stedman, Penn cell biologist Nancy Minugh Purvis and their colleagues were looking at a section of what they thought was "junk" DNA. However, they noticed a similarity with genes known to control production of a protein that causes skeletal muscles to contract.
It turned out that a particular gene had a flaw that disables a protein that influences the chewing and biting muscles.
Analysis of human genetic samples from around the world revealed that all people carry this mutation. Non-human primates like macaque monkeys and chimps do not, and they continue to have jaws that are about 10 times more powerful than humans'.
Further genetic sleuthing determined that the mutation appeared in a human ancestor about 2.4 million years ago.
Changes in muscle anatomy are well-known to alter the bones to which they attach. The exciting part of this is the mutation in the gene dates to exactly when this transition occurs in the fossil record.
The Penn researchers argue it is no coincidence that larger braincases and smaller teeth occurred at about the same time.
There is plenty of debate about whether those human ancestors were the first to use tools or even if there were more than one species of them in East Africa.
But scientists are certain that those early humans were the first in the family tree to have a brain larger maybe considerably larger than 500 cubic centimeters. Fossil skulls indicate that, over a few hundred thousand years, the next known human ancestor had a brain as large as 1,000 cubic centimeters. That means this ancestor, Homo erectus, had a braincase notably larger than the teeth and jaws.
The average brain size for people today is about 1,300 cubic centimeters. "We think it's logical to consider that the mutation's decrease in jaw-muscle size and force eliminated stress on the skull, which 'released' an evolutionary constraint on brain growth," Minugh-Purvis said.
Though the lack of this gene did not cause our cranial capacity to grow it did reduce the temporalis muscle size and allowed our brains to grow and our skulls to enlarge because of it.
To date none of the skulls dug up in Africa are identified as Chimpanzee ancestors even though they about the same size, except that some of them are larger.
What? We found chimpanzee fossils in 2005. Most of the fossils are classified as hominids because they show human characteristics such as a parabolic jaw shape and reduced canine/tooth size.
While some behavior can be shown through fossils (diet, etc.) we can gather environmental data from fossils. Human history is actually becoming more clear as we delve into not only the fossil record but other fields such as embryology and genetics which all independently converge on... evolution.
The law of parsimony (Ockham's razor) is a rule in science and philosophy stating that entities should not be multiplied needlessly.
Sorry but I don't subscribe to that joke of a law. If it were true, disease would still be caused by spirits because that is simpler an explanation than saying all these different species and strains of bacteria, viruses, and even genetic diseases are the cause.
Since the molecular basis for human evolution is unknown the miraculous interpolation remains the simplest explanation consistent with normative Biology.
Wrong. We've witnessed an lot of genes that is responsible for human development. We don't have tails because the gene for tale development is (usually) switched off and apoptosis reduces the tail that did develop.
We have the gene for tail growth, as is found in all mammals! In fact, the genes that control the development of tails in mice and other vertebrates have been identified (the Wnt-3a and Cdx1 genes). It is now known that down-regulation of the Wnt-3a gene induces apoptosis of tail cells during mouse development, and similar effects are observed in humans. Additionally, researchers have identified a mutant mouse that does not develop a tail, and this phenotype is due to a regulatory mutation that decreases the Wnt-3a gene dosage. Thus, current evidence indicates that the genetic cause of tail loss in the evolution of apes was likely a simple regulatory mutation that slightly decreased Wnt-3a gene dosage. Isn't it funny that God would give us a gene that we don't need?
With a cranial capacity nearly three times that of the chimpanzee the molecular basis for this giant leap in evolutionary history is still almost, completely unknown.
Though we've found nearly complete skulls that show an increase in cranial capacity from the 400cc of australopithecines to the average of 1100 in modern
Homo sapiens.
Changes in brain related genes are characterized by debilitating disease and disorder and yet our decent from a common ancestor with the chimpanzee would have had to be marked by a massive overhaul of brain related genes.
Here you go:
Researchers identify genes involved in evolution of brain development
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By Catherine Gianaro [/SIZE][/FONT]
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Medical Center Public Affairs[/FONT][/SIZE]
Researchers have identified two genes implicated in the dramatic expansion of the human cerebral cortexa development considered to be one of the hallmarks of human evolution.
The researchers, led by Bruce Lahn, Assistant Professor in Human Genetics, presented evidence that the pressure of natural selection has led to dramatic evolutionary changes in a gene called
Microcephalin and another gene called ASPM. Both are known to control brain size during development in humans.
The researchers decided to explore
Microcephalin and ASPM because mutant forms of these genes cause primary microcephaly, a developmental defect that affects humans. This disorder is marked by a severe reduction in the size of the brain, particularly the cerebral cortexthe part of the brain responsible for planning, abstract reasoning and other higher brain functions. The brains of people with primary microcephaly are otherwise normal, and other structures of the body seem unaffected.
The researchers traced the evolution of
Microcephalin and ASPM by comparing the genes sequences in a range of primates, including humans, as well as non-primate mammals. Specifically, the researchers sequenced the human, chimpanzee, gorilla, orangutan, gibbon, colobus monkey, squirrel monkey and lemur forms of the genes.
We chose these species because they were progressively more closely related to humans, said Lahn. For example, the closest relatives to humans are chimpanzees, the next closest are gorillas, and the rest go down the ladder to the most primitive.
The sequence of primates from human to lemur generally represents a progression from the most advanced to the more primitive. Chimpanzees are the closest, living genetic relative of humans, and the lemur represents the most primitive primate, having branched from the primate tree before the evolution of monkeys, apes and humans. To study the evolution of the genes in other mammals, the researchers also sequenced these genes from the dog, cat, cow, sheep, rat and mouse.
For each species, the researchers identified changes in both the
Microcephalin and the ASPM genes that altered the structure of the resulting proteins, as well as those that did not affect protein structure. Only those genetic changes that alter protein structure are likely to be subject to evolutionary pressure, Lahn said. Changes in the gene that do not alter the protein indicate the overall mutation ratethe background of random mutations from which evolutionary changes arise. Thus, the ratio of the two types of changes gives a measure of the evolution of the gene under the pressure of natural selection.
The researchers are continuing their studies to determine the biological function of the two genes, to better understand how their mutation could have led to the characteristic enlargement of the human brain. We want to know when was the last time that the lightning of evolution struck either one of these genes during human evolution, said Lahn. Was it 100,000 years ago, or a million years ago or half a million years ago? That would be fascinating to know from the viewpoint of understanding the history of evolution of the human brain.
http://chronicle.uchicago.edu/040429/brainsize.shtml
This hall of skulls jpg is used by the TO propaganda to create a homology illusion. When you look closer at the actuall skulls, and I have, the real differences start to jump out at you. If you only knew how many times I have debunked this empty attempt at viable proof.
I'll just check and see how well you've done
.
(A) Pan troglodytes, chimpanzee, modern
Chimpanzee of course, see image above for specific morphological differences.
(B) Australopithecus africanus, STS 5, 2.6 My Chimpanzee ancestor
(C) Australopithecus africanus, STS 71, 2.5 My Chimpanzee Ancestor
Okay, australopithicines were not chimpanzee ancestors. Claiming such nonsense shows you really can't tell the difference. Let's look at a chimpazee pelvis versus an australopithicine and a modern
Homo sapiens.
As you can see, Lucy (an australopithicine), has the short wide hips characteristic of humans in addition to a femur that curves inward to better support an upright body. Chimpanzee hips are long and the legs are straight which makes walking upright for long periods of time very difficult. Australopithicines are definitely not chimpanzee ancestors.
From the Smithsonian's article on Homo habilis:
An arbitrary lower limit had been set between 700cc and 800cc as the cutoff for the genus Homo. With an estimated cranial capacity of 680cc, Leakey and his colleagues chose to lower this number to 600cc...they chose a behavior- the ability to make stone tools-to help place OH 7 in Homo. This point relied on stone tools found in the same geologic horizon as the fossils.
Raymond Dart who's Taung Child had long been considered a chimpanzee skull came the suggestion for a name for the stone age ape man myth, Homo habilis.
Chimpanzee ancestor.
First of all, why did chimpanzee ancestors have larger cranial compacities than chimpanzees do today? Is it a result of the fall? Maybe chimpanzees are Cain's descendants since their ancestor
Homo habilis was capable of making stone tools and they cannot.
Chimpanzee ancestor
(F) Homo rudolfensis, KNM-ER 1470, 1.8 My
Most scientists do not think
Homo rudolfensis was an ancestor of modern
Homo sapiens.
I like this game, now it's my turn to play. What is the molecular mechanism responsible for this giant leap?
Here's an example for bipedalism.
Scholars have long thought that bipedality evolved gradually in response to the opening of the savanna. Recently, both parts of this concept have come into question. A variety of benefits of bipedality have been posited as responsible, but a trait can not evolve unless a useful mutation appears. Perhaps we need to stop wondering about selective pressures and consider what kind of mutation might be involved in forming a bipedal pelvis. Work on the evolution of development has shown that there are segmental control genes, alterations in which have large effects. These include the hox genes, of which there are four sets in humans, referred to as the HOX A, B, C, and D sequences. Changes in their activation in embryogenesis alter the identity of vertebrae and limb structure. An alteration in the control region of certain of the distal HOX D genes may well be responsible for the sudden appearance of bipedality by moving the boundary between the lumbar and sacral vertebrae, and so moving the position of the pelvis and lower limb origin. Pongids usually have three lumbar vertebrae; early hominids, 6. Pongids also have 48 chromosomes while we have 46. HOX D is located on our 2nd chromosome, the one that is a fusion of two pongid chromosomes. If that fusion altered the onset of perhaps HOX D 10, so that it switched on a couple of segments later, then the sacrum would form further down the vertebral column and might be shorter. In this paper I look at the chromosomal location of HOX D and examine the likelihood that the fusion of two panid chromosomes could have given rise to alterations in its control resulting in the abrupt appearance of bipedality and accompanying changes in the limbs and in the chela in which the HOX sequences are reused.
Try again. This is fun!
