P
PhilVaz
Guest
Ric << Yes, there is close similarity between chimp and human genes. The Oldsmobile and Buick have almost exactly the same parts, so one must have evolved from the other, just as evolution predicts. >>
You need to read that article (“Plagiarized Errors and Molecular Genetics”) I linked earlier. The copying or similarity is not just in the genes, but in the pseudo-genes which are non-functional.
A better analogy than yours would be to consider one car, say Car A, then we have two other Cars, Cars B and Cars C, while they both look somewhat like Car A, it is Car C that not only copies the outside and inside, but also the design MISTAKES and FLAWS in Car A.
Or take Book A, then another Book B that copies not only the words of Book A but the exact SPELLING MISTAKES in book A. We can conclude the author of Book B plagiarized Book A, and Book A is its “common ancestor” (as are those who copy A’s and B’s same mistakes later).
That’s what pseudo-genes are. They are mistakes or non-functional genes that are still copied through and passed forward. And that’s how we know humans and chimps had a common ancestor (i.e. through macroevolution) since we have not only almost identical DNA, but identical COPYING MISTAKES in our DNA. These MISTAKES are created by random mutations, but are still passed through during the copying process. At least that’s how I understand it.
See my summary of Theobald’s evidence which I turn into questions here.
molecular sequence evidence
Why is a full 45% of our genome composed of transposons, which serve no known function for the individual except to cause a significant fraction of genetic illnesses and cancers? Why are 21% of the human genome pseudogenes which serve no function? Why in humans is there one functional GDPH gene, but there are at least twenty GDPH pseudogenes? Why in mice are there approximately 200 GDPH pseudogenes, none of which are necessary?
Why do humans and chimpanzees have the exact same cytochrome c protein sequence, when the chance occurrence of this is conservatively less than 1 out of 10^93 ? Why do human and chimpanzee cytochrome c proteins differ by only about 10 amino acids from all other mammals, when the chance occurrence of this in the absence of a hereditary mechanism is less than 1 out of 10^29 ?
Why is bat cytochrome c much more similar to human cytochrome c than to hummingbird cytochrome c? Why is porpoise cytochrome c much more similar to human cytochrome c than to shark cytochrome c? Why does the phylogenetic tree data constructed from the cytochrome c data exactly recapitulate the relationships of major taxa as determined by the completely independent morphological data?
Why are the cytochrome c proteins in chimps and humans exactly identical? Why do the two DNA sequences that code for cytochrome c in humans and chimps differ by only one base, a 0.3% difference, even though there are 10^49 different sequences that could code for this protein?
Why are there very many examples of shared pseudogenes between primates and humans, with one hemoglobin, the ψη-globin pseudogene shared among the primates only, in the exact chromosomal location, with the same mutations that render it nonfunctional? Why do chimps and humans both share the same eight bp deletion in the steroid 21-hydroxylase pseudogene that renders it nonfunctional?
The correct answer to these questions: we are related by descent with modification and share common ancestors with all of life (i.e. macroevolution is true).
Phil P
You need to read that article (“Plagiarized Errors and Molecular Genetics”) I linked earlier. The copying or similarity is not just in the genes, but in the pseudo-genes which are non-functional.
A better analogy than yours would be to consider one car, say Car A, then we have two other Cars, Cars B and Cars C, while they both look somewhat like Car A, it is Car C that not only copies the outside and inside, but also the design MISTAKES and FLAWS in Car A.
Or take Book A, then another Book B that copies not only the words of Book A but the exact SPELLING MISTAKES in book A. We can conclude the author of Book B plagiarized Book A, and Book A is its “common ancestor” (as are those who copy A’s and B’s same mistakes later).
That’s what pseudo-genes are. They are mistakes or non-functional genes that are still copied through and passed forward. And that’s how we know humans and chimps had a common ancestor (i.e. through macroevolution) since we have not only almost identical DNA, but identical COPYING MISTAKES in our DNA. These MISTAKES are created by random mutations, but are still passed through during the copying process. At least that’s how I understand it.
See my summary of Theobald’s evidence which I turn into questions here.
molecular sequence evidence
Why is a full 45% of our genome composed of transposons, which serve no known function for the individual except to cause a significant fraction of genetic illnesses and cancers? Why are 21% of the human genome pseudogenes which serve no function? Why in humans is there one functional GDPH gene, but there are at least twenty GDPH pseudogenes? Why in mice are there approximately 200 GDPH pseudogenes, none of which are necessary?
Why do humans and chimpanzees have the exact same cytochrome c protein sequence, when the chance occurrence of this is conservatively less than 1 out of 10^93 ? Why do human and chimpanzee cytochrome c proteins differ by only about 10 amino acids from all other mammals, when the chance occurrence of this in the absence of a hereditary mechanism is less than 1 out of 10^29 ?
Why is bat cytochrome c much more similar to human cytochrome c than to hummingbird cytochrome c? Why is porpoise cytochrome c much more similar to human cytochrome c than to shark cytochrome c? Why does the phylogenetic tree data constructed from the cytochrome c data exactly recapitulate the relationships of major taxa as determined by the completely independent morphological data?
Why are the cytochrome c proteins in chimps and humans exactly identical? Why do the two DNA sequences that code for cytochrome c in humans and chimps differ by only one base, a 0.3% difference, even though there are 10^49 different sequences that could code for this protein?
Why are there very many examples of shared pseudogenes between primates and humans, with one hemoglobin, the ψη-globin pseudogene shared among the primates only, in the exact chromosomal location, with the same mutations that render it nonfunctional? Why do chimps and humans both share the same eight bp deletion in the steroid 21-hydroxylase pseudogene that renders it nonfunctional?
The correct answer to these questions: we are related by descent with modification and share common ancestors with all of life (i.e. macroevolution is true).
Phil P