Genetic proof for the origin of man


This is a brief summary of a 26-page article by Edward E. Max, M.D., Ph.D.:

Plagiarized Errors and Molecular Genetics

Another argument in the evolution-creation controversy

Scource: www.talkorigins.org/faqs/molgen - Copyright © 1986-2002



In this article, E.E.Max describes some discoveries from his own field of
molecular genetics. He shows how they provide evidence for evolution that is
both convincing and conceptually simple enough for the interested layperson
to appreciate.

In the context of this article "creationist" designates the specific belief
that different species or "kinds" were created seperately, not the general
belief that a creator is responsible for all of creation, no matter whatever
mechanisms he used. Whether an "evolutionist" does or does not believe in a
Creator is not specified.

Species similarities and their different interpretations

Present-day humans and chimpanzees, despite obvious external and behavioral
differences, have extremely similar internal organs and physiological
functions; indeed their genes are more than 98% identical. However, the
similarities between species in anatomy and protein structure can be
interpreted in two entirely different ways:

· "Creationists" say that apes and humans were created independently
but were designed with similar features so that they would function
similarly.

· Evolutionists say that the similarity between features of, for
example, humans and apes reflects the fact that these features were
inherited from a common ancestor; that is, the similar features of humans
and apes are determined by modern copies of genes that once existed in a
species that was ancestral to both apes and humans. Just as the resemblance
between two siblings suggests a common parentage, resemblance between
species suggests common ancestors.
Evolutionists believe that humans, gorillas, and chimpanzees evolved from a
common ancestor: an ape-like creature that lived perhaps five to ten million
years ago, rather recently on the geological time scale. Species less
similar to humans than are apes - mice, for example - are believed to have
branched off millions of years earlier from a common primitive mammalian
ancestor.

Both the gene copying and the independent creation views seem consistent
with the similarity data, but which view is correct?

A possible rationale to resolve the deadlock

One way to distinguish between copying and independent creation is suggested
by analogy to the following two cases from the legal literature: In 1941 the
author of a chemistry textbook brought suit charging that portions of his
textbook had been plagiarized by the author of a competing textbook. In 1946
the publisher of a trade directory for the construction industry made
similar charges against a competing directory publisher.

In both cases, mere similarity between the contents of the alleged copies
and the originals was not considered compelling evidence of copying.

After all, both chemistry textbooks were describing the same body of
chemical knowledge (the books were designed to "function similarly") and
both directories listed members of the same industry, so substantial
resemblance would be expected even if no copying had occurred.

However, in both cases errors present in the "originals" appeared in the
alleged copies. The courts judged that it was inconceivable that the same
errors could have been made independently by each plaintiff and defendant,
and ruled in both cases that copying had occurred.

The principle that duplicated errors imply copying is now well established
in copyright law. In recognition of this fact, directory publishers
routinely include false entries in their directories to trap potential
plagiarizers.

Can "errors" in modern species be used as evidence of "copying" from ancient
ancestors?

In fact, the answer to this question appears to be "yes," since recent
molecular genetics investigations have uncovered some examples of the same
"errors" present in the genetic material of humans and apes. To understand
these findings it is necessary to know a little about DNA, the chemical
molecule in which genetic information is stored.

DNA basics

Inside the cell's nucleus, most of the DNA exists as a double helix. The
genetic information is stored in the sequences of nucleotide bases (A, T, G
or C) that form the rungs of a ladder. Each rung is formed by a pair of
nucleotide bases touching each other, one base attached to one strand
backbone, and the other attached to the other strand backbone. An "A"
nucleotide always pairs with a "T," and a "G" always pairs with a "C." In
order to synthesize a protein, the cell reads the genetic information of the
gene for that protein by "transcribing" a molecule of RNA from the gene. The
RNA sequence is then "translated" into protein.

When a cell divides, the entire sequence of its DNA must be duplicated into
two faithful copies of the original; one copy goes to each of the "daughter"
cells created by the division. Occasionally, errors occur in this copying
mechanism, creating "mutations" in the DNA sequence. Such changes can occur
in most cells in the body - liver, skin, muscle, etc. - without being
transmitted to offspring when the organism reproduces. However, when
mutations occur in the egg or sperm or, more generally in "germline cells",
they can be passed on to future generations.

DNA errors

Recombinant DNA technology has in recent years allowed scientists to
determine the sequence of nucleotides in segments of DNA from many species,
and several billion nucleotides' worth of information has accumulated. These
sequences have vastly increased our understanding of how genes normally
function; but, more to the point of this article, they have provided a
treasure trove of genetic "errors" that are potential clues to the analysis
of copying discussed earlier.

In this context I use the word "error" to include any DNA feature that we
have good reason to believe (1) originated from a genetic "accident"; (2)
serves no benefit to the organism carrying the features; and (3) therefore
cannot reasonably be interpreted as having been "designed."

Unitary pseudogenes

Guinea pigs and primates, including humans, get sick unless they consume
ascorbic acid in their diet. For humans and guinea pigs, ascorbic acid is
thus a vitamin (vitamin C), while most other species can synthesize their
own ascorbic acid and thus do not require this molecule in their diet. The
reason humans and guinea pigs cannot manufacture their own ascorbic acid is
that they lack a functional gene encoding the enzyme protein known as
L-gulono-gamma-lactone oxidase (GLO), which is required for synthesizing
ascorbic acid. In most mammals functional GLO genes are present, inherited -
according to the evolutionary hypothesis - from a functional GLO gene in a
common ancestor of mammals. According to this view, GLO gene copies in the
human and guinea pig lineages were inactivated by mutations. Presumably this
occurred separately in guinea pig and primate ancestors whose natural diets
were so rich in ascorbic acid that the absence of GLO enzyme activity was
not a disadvantage - it did not cause selective pressure against the
defective gene.



· Molecular geneticists who examine DNA sequences from an
evolutionary perspective know that large gene deletions are rare, so
scientists expected that non-functional mutant GLO gene copies - known as
"pseudogenes" - might still be present in primates and guinea pigs as relics
of the functional ancestral gene. Pseudogenes are called "unitary" if they
arose from single, rather than duplicated genes, such that no functional
copy remains.

· In contrast, "Creationists" believe that humans and guinea pigs
were each created independently of all other species and must have been
"designed" to function without GLO. If this were true, these two species
would not be expected to carry a defective copy of the GLO gene.

In fact, GLO pseudogenes have been detected in both guinea pigs and humans,
consistent with the evolutionary view. The kinds of mutations found in the
human and guinea pig pseudogenes are typical of the ones seen in genetic
diseases.

Endogenous retroviruses

Infectious retroviruses were discovered as agents of human disease and have
been intensively studied. Infectious retroviruses include HTLVI, which
causes a kind of leukemia in humans, and HIV, which causes AIDS. These
viruses typically infect specific kinds of white blood cells - lymphocytes -
and insert reverse-transcribed copies of their RNA genes into the DNA of
these cells.

Soon after the discovery of infectious retroviruses, scientists noticed that
similar sequences were present in the DNA of many mammalian species,
including humans; these copies are called endogenous retroviruses, and
presumably represent the consequences of ancient retroviral infections of
germline cells.

In human DNA there are about 8 different classes of endogenous retroviruses
with members of each class varying in number from one or two to more than 50
copies. Essentially all of these endogenous retroviruses contain mutations
that would disrupt the function of their genes, as would be expected if they
inserted millions of years ago with no selective pressure to maintain the
function of the genes.

How ancient errors can persist in modern species

How could non-functional sequences, arising in a germline cell of a
particular individual, come to be preserved in all individuals of a species?
The extra burden of carrying along even a large pseudogene sequence - for
example, 100,000 nucleotides - is insignificant for a mammalian cell with
approximately three billion nucleotides' worth of information. In any case,
there is no known "proofreading" mechanism by which the cell might
distinguish non-functional from functional DNA and selectively eliminate
what it does not need. Functionless DNA sequences that scientists have
inserted into the DNA of mice or other species are faithfully passed to
descendants, and naturally occurring pseudogenes and retroposons apparently
behave similarly. Retroposons derive from non-viral RNA accidentally
reverse-transcribed into DNA that is inserted back ("retroposed") at some
random position of the cell's DNA. Although the high content of apparent
"junk DNA" was initially surprising when it was discovered, our current
understanding of the mechanisms of genome expansion (duplication and
insertion) and the apparent lack of significant selective pressure to
minimize genome size combine to make the accumulation of useless sequences
in our DNA seem inevitable.

The crucial observation relating the discovery of pseudogenes and
retroposons to the theory of evolution is this: some pseudogenes and
retroposons are shared between different species, as though they were copied
from a pseudogene or retroposon in a common ancestor:

Shared unitary pseudogenes

Many of the unitary pseudogenes in humans are shared with other primates. By
"shared" I mean more than simply that the same gene is inactive in two
different species, since that situation could result if the corresponding
genes of the two species were inactivated separately by independent
mutations.

Instead, in all the examples I describe, the pseudogenes in primates carry
many of the same crippling mutations found in the corresponding human
pseudogenes.

Since independent random mutations would not be likely to be identical in
two different species, the identically mutated pseudogenes are strong
evidence that the mutations occurred in a common ancestral species.

For the example of the GLO unitary pseudogene of humans, it is known that
vitamin C is required in the diet of other primates (though not for other
mammals except guinea pigs).

The theory of evolution would make the strong prediction that primates
should also be found to have GLO pseudogenes and that these would carry
similar crippling mutations to the ones found in the human pseudogene.

A test of this prediction has recently been reported. A small section of the
GLO pseudogene sequence was compared from human, chimpanzee, macaque and
orangutan.

All four pseudogenes were found to share a common crippling single
nucleotide deletion that would cause the remainder of the protein to be
translated in the wrong triplet reading frame.

· The RT6 gene encodes a protein of about 230 amino acids expressed
on the surface membrane of T lymphocytes of rodents; both the human
pseudogene and its chimpanzee homolog contain mutations producing the same
three stop codons that would prevent the synthesis of an RT6 protein.

· Several of the human odorant receptor pseudogenes are found in
other primates, and share the same defects as the human pseudogenes.

· The human NPY1 receptor pseudogene shares a critical frameshift
mutation with primate homologs.

· The human urate oxidase pseudogene shares three crippling mutations
with the chimpanzee and orangutan pseudogenes.

Conclusion: shared genetic errors prove common descent!

All of the examples of functionless sequences shared between humans and
chimpanzees reinforce the argument for evolution that would be compelling
even if only one example were known. This argument can be understood by
analogy with the legal cases discussed earlier in which shared errors were
recognized as proof of copying. The appearance of the same "error" - that
is, the same useless pseudogene or retroposon or endogenous retrovirus at
the same position in human and ape DNA - cannot logically be explained by
independent origins of the two sequences.

The "creationist" argument - that similarities in DNA sequence simply
reflect the creator's plans for similar protein function in similar
species - does not apply to sequences that do not have any function for the
organism that harbors them. The possibility of identical genetic accidents
creating the same two pseudogene or retroposon or endogenous retrovirus
sequences independently in two different species by chance is so unlikely
that it can be dismissed.

As in the copyright cases discussed earlier, such shared "errors" indicate
that copying of some sort must have occurred. Since there is no known
mechanism by which sequences from modern apes could be copied into the same
position of human DNA or vice versa, the existence of shared pseudogenes or
retroposons leads to the logical conclusion that both the human and ape
sequences were copied from ancestral sequences that must have arisen in a
common ancestor of humans and apes.

At the present stage, the evidence suggests what to me is an awesome notion:
like a biological Rosetta Stone or Dead Sea Scroll, our own DNA - an
Encyclopedia Brittanica's worth of information in every cell of our body -
contains a record of the past which we are just now learning to read.
This record, reflecting millions of years of genetic history, includes the
relics of ancient genetic accidents that occurred before our ape-like
ancestors roamed the plains of Africa, relics that we now share with other
descendants of those same ancestors: modern gorillas and chimpanzees.

Two objections

In higher organisms, genes are composed of various shorter pieces, called
exons. After transcription, the pieces in-between, called "introns", are cut
out, while the exons are spliced together for translation. After this
processing, the RNA may accidentally be reverse-transcribed and inserted
into the cell's DNA, producing a "processed pseudogene" - which is not
needed.

Objection: Some processed "pseudogenes" are functional, so they could be
examples of "similar design for similar function!"

Several examples of this possibility have been reported, and these could be
interpreted as "similar design for similar function." But these examples
share a feature that clearly distinguishes them from the hundreds of
examples of useless processed pseudogenes reported: they lack crippling
mutations that would preclude function, and thus remain capable of encoding
a useful protein.

Objection: If all these sequences were really nonfunctional, they would have
been eliminated over evolutionary time!

This argument reflects ignorance of the facts discussed above. To repeat: no
mechanism is known by which non-functional DNA sequences might be
distinguished from functional ones and targeted for elimination by cellular
enzymes. In bacteria there is selective pressure for short, rapidly
replicating DNA, but this is not true for mammalian chromosomes, in which
genes are widely separated from one another and in which nonfunctional
regions apparently constitute 90-95% of the DNA.

In the original article E.Max goes much more into detail, explains several
other categories of functionless genetic sequences and gives many more
examples for "DNA errors", which humans share with other mammals. He also
deals with other possible objections: www.talkorigins.org/faqs/molgen

Read more about

Creation and Evolution
The original text of the bible and natural science

www.urzeitundendzeit.de/creation_and_evolution.htm

Armin








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