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Has anyone ever actually done an equation to work out human evolution?
Actually, yes. Neutral mutations, those that do not change or only slightly change phenotype, accumulate at a probabilistic rate. Therefore, one can use math equations to figure out the mutation rate needed to produce the differences seen in human and chimp pseudogenes. Psuedogenes are used because mutations that occur in these genes are more than likely neutral.
The next step is to observe the mutation rate in humans. The best way to do this is to use disease genes. What you do is measure the rate at which the diseases occur within a specific population, preferably a population that has universal health care so that you know that the disease rate is accurately reported. You can then extrapolate the mutation rate within these genes to the genome at large.
So what happens when you compare these two numbers? They match.
Hum Mutat. 2003 Jan;21(1):12-27.Links Direct estimates of human per nucleotide mutation rates at 20 loci causing Mendelian diseases.
Kondrashov AS.
National Center for Biotechnology Information, NIH, Bethesda, Maryland 20892, USA. Kondrashov@ncbi.nlm.nih.gov
I estimate per nucleotide rates of spontaneous mutations of different kinds in humans directly from the data on per locus mutation rates and on sequences of de novo nonsense nucleotide substitutions, deletions, insertions, and complex events at eight loci causing autosomal dominant diseases and 12 loci causing X-linked diseases. The results are in good agreement with indirect estimates, obtained by comparison of orthologous human and chimpanzee pseudogenes. The average direct estimate of the combined rate of all mutations is 1.8x10(-8) per nucleotide per generation, and the coefficient of variation of this rate across the 20 loci is 0.53. Single nucleotide substitutions are approximately 25 times more common than all other mutations, deletions are approximately three times more common than insertions, complex mutations are very rare, and CpG context increases substitution rates by an order of magnitude. There is only a moderate tendency for loci with high per locus mutation rates to also have higher per nucleotide substitution rates, and per nucleotide rates of deletions and insertions are statistically independent on the per locus mutation rate. Rates of different kinds of mutations are strongly correlated across loci. Mutational hot spots with per nucleotide rates above 5x10(-7) make only a minor contribution to human mutation. In the next decade, direct measurements will produce a rather precise, quantitative description of human spontaneous mutation at the DNA level. Published 2002 Wiley-Liss, Inc. emphasis mine
__________________ "Since YAC [Young-Age Creation] epistemology accepts Biblical claims over physical evidence and human reason, logical or evidential arguments for evolution and/or against YAC are likely to be ineffective in converting most YACists."--Kurt Wise
Why don't humans really evolve that much any longer?
We do. Large, morphological change requires many thousands of years, something most humans don't live long enough to see .
But we have evolved. For example, most humans are lactose intolerant, simply because we never used to drink milk beyond our infancy. But in Europe, only 10% of people are lactose intolerant: the European population has evolved and diminished the number of people who can't drink milk. But, in Native American tribes, lactose intolerance is universal: 100% of people can't drink milk. This is because they never really drank milk, so they never experienced the same selection pressures as humans.
And, to invoke the dark and terrible taboo that is race, it is undeniable (if politically incorrect) that there are racial differences:
Superficially different, but different nonetheless. The human species has evolved as it migrated about the world: those whose ancestors stayed in Africa maintained their dark-pigmented skin, while those whose ancestors migrated to the cold North evolved pale skin.
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- Stargate: SG1
What can be asserted without reason, can be denied without reason.
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"A casual stroll through the lunatic asylum shows that faith does not prove anything."
But other species are supposed to have evolved far more and they don't even have enough generations available to do it in, humans, for example. Between humans and a putative human-ape ancestor ten million years ago there are a maximum of perhaps one million generations, depending on the reproductive age at different stages. During that e-coli experiment, there was time for 653 mutations by generation 40,000, the later ones being mostly not helpful to the bacteria, divide 1 million generations by 40,000 we get 25 minor changes (eg. the abilty to digest something not previously able to handle), surely at a minimum to go from ape ancestor to human would take some 30 million minor changes, or 19,590,000,000 mutations, according to that experiment, there would happen only 16,325 mutations during that amount of time. Is it possible?
Not enough time and too few mutations? I too had the same concerns, until I came across 'Evo-Devo' (evolutionary and developmental biology) and Sean Carroll's book "Endless Forms Most Beautiful". Before the days of gene sequencing I thought the differences between chimps and humans must be due to beneficial mutations in hundreds of the basic protein-coding genes. But that's not what was found.
Pete Harcoff explained why mutation rates of humans and bacteria can't be directly compared. There's another consideration. Multicellular organisms usually consist of cells that are differentiated to provide form (morphology) and function (physiology). The protein-coding genes that generate an organism's essential biochemistry and basic structure are themselves under the control of regulatory genes. In 'higher' animals, cell and tissue differentiation take place during embryonic development from genes that control the body plan. Since the timing and activity of these genes gives the body its specific shape and physiology, the regulatory factors that control these genes are obviously very important. Such would not be the case in E coli because it's morphology is too simple.
Here's a couple of extracts from papers that discuss the subject:-
A very important feature of the regulatory DNA code for animal development is that much of it is used to control expression of genes encoding regulatory proteins, in addition to the many genes encoding the structural proteins of which the animal will be built. In that each cis-regulatory element processes multiple inputs, it interacts with multiple transcription factors produced by multiple distinct genes. And each transcription factor interacts with multiple cis-regulatory elements. From these elemental facts the genomic regulatory code for development can be seen to generate a system of interactions that has the architecture of a network (rather than, say, a simple linear or branching pathway). Each node of a developmental gene regulatory network (GRN) thus consists of a gene encoding a transcription factor or a signaling component, together with the cis-regulatory module(s) controlling expression of that gene. As do transcription factors, signaling components may immediately affect the program of gene expression downstream of their own transcription. The architecture of the GRN can be considered to consist of the functional linkages among the nodes of the network. These linkages connect the output of the gene at each node to its target genes, where they serve as cis-regulatory inputs.
ht*p://w*w.pnas.org/content/100/4/1475.full
Gene regulation can therefore be influenced by a huge number of factors, including the distance of regulators from their target gene, and this can even be affected by so-called 'junk' DNA. This is seen as the foundation of animal diversity.
In general, a large number of different genes are involved in the development of phenotypic characters, and changes in the coordination of temporal and spatial expression of these genes in the developmental process play important roles in evolution. There are usually several signaling pathways for producing the same end character, and complex gene interaction occurs as a form of gene regulatory networks (42–44). The number of genes involved in these signaling pathways or genetic networks generally increases as the phenotypic character involved becomes more complex, and this increase in gene number is ultimately caused by gene duplication (45). For this reason, gene duplication is the fundamental process of generating complex organisms (26, 46–48).
ht*p://w*w.pnas.org/content/104/30/12235.full
Almost all of these mutations were beneficial ... beneficial substitutions were surprisingly uniform over time.
Perhaps because the E. Coli were bred in labartory environments? Most controlled experiments try to mimimise uncontrollable variables - so the E. Coli were not exposed to the effects of natural selection?
Perhaps because the E. Coli were bred in labartory environments? Most controlled experiments try to mimimise uncontrollable variables - so the E. Coli were not exposed to the effects of natural selection?
The experiment was on evolution. Why would they not expose E. coli to natural selection? How weren't they exposed? They were left to breed as they saw fit, which necessarily entails natural selection.
__________________
A scientific man ought to have no wishes, no affections, -- a mere heart of stone.
- Charles Darwin
"I am a scientist... when I find evidence that my theories are wrong, it is as exciting as if the evidence proved them right."
- Stargate: SG1
What can be asserted without reason, can be denied without reason.
- Anon
"A casual stroll through the lunatic asylum shows that faith does not prove anything."
The experiment was on evolution. Why would they not expose E. coli to natural selection? How weren't they exposed? They were left to breed as they saw fit, which necessarily entails natural selection.
In 1988 an associate professor started growing cultures of Escherichia coli ... Sequencing genomes of various generations of the bacteria, which had been frozen periodically over the years.
Here we sequence genomes sampled through 40,000 generations from a laboratory population of Escherichia coli.
The E. coli were grown in a controlled environment, which is quite the opposite to natural selection.
The E. coli were grown in a controlled environment, which is quite the opposite to natural selection.
I think you are slightly confused about what "Controlled" means in the context of science. "Controlled" simply means that there were no random, outside variables like contaminants allowed to grow in the medium.
Controlled and Natural Selection are not opposites.
I think you are slightly confused about what "Controlled" means in the context of science. "Controlled" simply means that there were no random, outside variables like contaminants allowed to grow in the medium.
But nature itself is full of frequent and often unpredictable changes. It's the organisms' ability to adapt to these changes which natural selection is based on. The website OP provided specifically mentioned that the environment was constant.
The E. coli were grown in a controlled environment, which is quite the opposite to natural selection.
The environment was controlled - the selection wasn't. There was no guarantee whether or not one particular line would adapt to a given set of parameters.
And just because there was a controlled environment, doesn't mean there weren't conditions there the E.Coli could adapt to - citrate feed being one of them, as the initial line couldn't digest that, but some lines eventually evolved the ability to do so.
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Last edited by Cabal; 23rd October 2009 at 09:52 PM.
But nature itself is full of frequent and often unpredictable changes. It's the organisms' ability to adapt to these changes which natural selection is based on. The website OP provided specifically mentioned that the environment was constant.
The fact that the environment was static doesn't negate the fact that natural selection still occurred. They had an environment that was rich in citrate, and so the evolution of a Cit+ phenotype was naturally advantageous. Natural Selection.
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