This is no more ethically troubling than a set of pigs which have the
entire human immune system genetically spliced into them.
I would add as an aside, that those who are claiming that the mtDNA work
last year with Neanderthal proves that Neanderthal couldn't be our ancestor
might easily be proven wrong. Does anyone seriously think that a human
egg, with all human mitochondria replaced by gorilla mitochondria would not
be able to fuse with a human sperm and give rise to a human with gorilla
mitochondria? While this would be unethical, I have no doubt that it could
be carried out successfully.
>
>> What I noticed (most ironically) is that this particular gene, the first
>> major one known to be clearly human, does indeed go the direction that
>> anti-evolutionists perfer. The human sialic acid is a degenerate form when
>> compared with the better ape version. Thus, we can conclude that our
>> evolution obeys the "anti-evolutionary claims" and represents a loss of
>> information. We have indeed lost information. God created the apes and we
>> have degenerated from them. Now that we know that we are lesser than the
>
> Can you really say it's a "degenerate" form and not simply an alternate
>form. After all, it would presumably would have some beneficial trade-off
>in order to be naturally selected.
Not entirely true. This is a trap that young-earth/antievolutionists fall
into. The assumption is that a given mutation must be beneficial. But in
genetics two bad mutations if they occur singly, may be beneficial if they
occur together. Consider Antibiotic resistance in the bacteria:
"They are one of medicine's biggest headaches: bacteria that have evolved
reisitance to those former wonder drugs, antibiotics. Now it appears
-contrary to everyone's hopes and microbiologists' expectations-these
troublesome microbes will remain resistant long after doctors stop
prescribing the drugs." P. 575
"'Theoretically, the genes responsible for resistance are supposed to
adversely affect the bacteria's fitness.' Levin explains. 'You're altering
a gene's normal function and therefore expect it to have a disadvantage.
"But a random survey last year of Escherichia coli bacteria collected
from a day-care center in Atlanta by Levin and an Emory undergraduate,
Bassam Tomah, suggested that the theory may not hold up. In a quarter of
the bacteria sampled from the diapers of 25 infants, the researchers found
strains of E. coli still resistant to streptomycin, an antibiotic doctors
have rarely used for the last 30 years. Adding to this puzzle are bacteria
in Richard Lenski's long-term evolution study at Michigan State University
in East Lansing. These E. coli originally carried a streptomycin-resistance
gene called rps, which is known to markedly reduce the bacteria's fitness.
Yet, after evolving in an antibiotic-free environment for 10 years, or
20,000 generations, Lenski's bacteria are still streptomycin-resistant.
'Why didn't' that gene revert to its sensitive state, when it only required
the change of a single DNA base?' askes Levin.
"To find out, Levin's colleauges Stephanie Schrage and veronique Perrot
allowed laboratory cutlures of E. coli with rpsL mutations to evolve in an
antibiotic-free medium for 16 days or 160 generations. They then completed
these evolved bacteria against drug-sensitive E. coli and found that they
are almost as fit. 'That suggests that they evovled a compensatory
mutation,' says Levin-a second genetic mutation that makes up for the loss
of fitness from the first.
"Schrage and Perrot, with Levin and Nina Walker, confirmed that suspicion
by making their evolved E. coli strain drug-sensitive again. They replaced
the bacteria's streptomycin-resistant rpsL gene with a sensitive version of
the gene, then set this genetically altered strain and the resistant strain
against each other ina another fitness-competition bout. The genetically
altered E. coli failed miserably-implying that the compensatory mutation
reduced its fitness when not paired with the resistance gene.
"The interaction between the two mutations would act as a kind of ratchet,
preventing bacteria from reverting to sensitivity. 'The compensatory
mutations establish an 'adaptive valley' that virtually precludes that
population of resistant bacteria from returning to drug sensitivity,'
explains Levin. And that explains why the bacteria in Lenski's lab and
possibly those in the children's diapers have not lost their resistance.
'Those that revert, that make that one change, are at a disadvantage,'
explains Levin. The team is now trying to identify the gene tthatcarries
this compensatory mutation."
"Levin suspects that the same kind of compensatory mtuations 'will almost
certainly be found in other resistant bacteria.' But already, the findings
have 'clear, practical-and rather frightening-implications,' says Marlene
Zuk, an evolutionary biologist at the University of California, Riverside.
'It's not enough to stop using antibiotics; the bacteria aren't going to
revert to what they were before'-and antibiotics that have lost their
effectiveness won't become powerful weapons again."
~ Virginia Morell, "Antibiotic Resistance: Road of No Return," Science,
278(1997):575-576.
glenn
Adam, Apes and Anthropology
Foundation, Fall and Flood
& lots of creation/evolution information
http://www.isource.net/~grmorton/dmd.htm