Re: Evolution: A few questions

Dick Fischer wrote:
>Peter Ruest, wrote:
>>The spontaneous generation of information by means of natural selection
>>of random mutations does occur, but each such step of selection is just
>>a yes/no "answer" of the environment to the "question", "Is this ok?" of
>>the organism.
>
>I believe it is entirely possible that environment factors play an active
>role in eliciting change in the genetic mix upon which selection can act.

The influences of environmental factors on the evolutionary processes
are more complex than simple mutation and selection, as can be seen in
what follows. What I formulated above is just the simple basics of
evolution. But whatever these more complex processes contribute to the
phenotypes in a population, the environment's "answer" remains at most
one bit - yes/no for each phenotypic result. The increased complexity of
the "question" may be expected to slow down the fixation of any mutation
(usually pleiotropic - having various effects) possibly selected, if
any. Such more complex evolutionary steps hardly speed up the
acquisition of information usable to build novel systems. Environmental
factors tend to make evolution more difficult, not easier.

>This was in my book:
>
>Antibiotics experts have long recognized the adaptive capacity in microbes
>that have developed immunities to the drugs designed to wipe them out.
>Penicillin was introduced in the early 1940's. Soon after the infectious
>disease-causing bacteria were exposed to penicillin, they began
producing an
>enzyme called beta-lactamase, which destroys penicillin and related
>antibiotics.

Bacteria get their new anti-antibiotics (such as beta-lactamase) from
other microorganisms by horizontal gene transfer, usually nicely
packaged on a plasmid for ready use. There is quite a lot of horizontal
gene traffic among microorganisms (Dutta C., Pan A., "Horizontal gene
transfer and bacterial diversity", Journal of Bioscience 27 (Suppl.1)
(2002), 27-33). An enzyme (like beta-lactamase) cannot evolve _de novo_
within the short time between our using an antibiotic and the attacked
bugs' coming up with an antidote which makes them resistant. It is much
more likely that an antibiotic and its antidote evolved hand-in-hand in
the same bug - after all the producer itself needs to be immune against
it. Chemical warfare, including protection against the poison used, has
not been invented by humans.

Up to now, there is no information about the evolution of any
anti-antibiotic (like beta-lactamase), regarding the question of where
and how it evolved originally.

There are other cases (streptomycin) where resistance is produced by
means of a mutation damaging the ribosome in such a way that the
antibiotic cannot attack it any more (cf. Melançon P., Lemieux C.,
Brakier-Gingras L., "A mutation in the 530 loop of Escherichia coli 16S
ribosomal RNA causes resistance to streptomycin", Nucleic Acids Research
16 (1988), 9631-9639). In any case, appearance of resistance against
antibiotics is a very bad example for demonstrating the evolution of a
novel function - it is nothing of the sort -, although it is staple in
textbooks.

>In the early 1980's broad-spectrum beta-lactams were launched to kill
>drug-resistant bacteria. But the bacteria responded by mutating the gene
>encoding its defensive enzyme so that it now can ward off these drugs too.
>
>George Jacoby, a specialist in infectious diseases at Massachusetts
General
>Hospital, remarked, "Bugs are always figuring out ways to get around the
>antibiotics we throw at them. They adapt and come roaring back."

Not being in medicine, I don't know what exactly "broad-spectrum
beta-lactams" are; I assume they are differently modified penicillins
(possibly a mixture of a series of these), but all of them retaining the
original lactam ring of penicillin. It is this ring which is split by
the enzyme beta-lactamase, inactivating the penicillin. Therefore it is
probably not too difficult to mutate an available beta-lactamase in such
a way as to become active for a different lactam, like a modified
penicillin (cf. Barlow M., Hall B.G., "Predicting evolutionary
potential: in vitro evolution accurately reproduces natural evolution of
the TEM [beta]-lactamase", Genetics 160 (2002), 823-832). Not much of
novel evolution here, either.

>Researchers also know that certain genes have a DNA repair function. They
>even know there are several DNA repair pathways. Some genes are
capable of
>repairing DNA without making error, while other genes, in their words,
"are
>prone to make mistakes." It is suspected strongly that these latter genes
>that repair DNA with new coded information cause mutations which
contribute
>to genetic change.

Yes, this is one way of producing mutations. There are others. These
various DNA repair pathways are present in all bacteria (and all other
organisms have similar ones). Error-prone DNA repair is a common stress
response pathway (Bjedov I., Tenaillon O., Gérard B., Souza V., Denamur
E., Radman M., Taddei F., Matic I., "Stress-induced mutagenesis in
bacteria", Science 300 (2003), 1404-1409). By producing more mutations
than normal, a larger percentage of a population gets a lethal damage,
but among the survivors, the chance of producing a change conducive to
better survival under the stressing conditions is somewhat higher. In
this way, a process damaging some bacteria may improve the survival
chances of the entire population. The presence of an antibiotic, of
course, is a stress situation.

If an advantageous mutation happens to arise, it will usually not
produce anything new, but mobilize some function which was already
present but not active under normal conditions. One famous case is the
"evolution" of cellobiose utilization in E.coli under starvation
conditions (Kricker M., Hall B.G., "Directed evolution of cellobiose
utilization in Escherichia coli K12", Molecular Biology and Evolution 1
(1984), 171-182; Hall B.G., Betts P.W., Kricker M., "Maintenance of the
cellobiose utilization genes of Escherichia coli in a cryptic state",
Molecular Biology and Evolution 3 (1986), 389-402; Hall B.G., "Directed
evolution of a bacterial operon (my favorite molecule)", BioEssays 12
(1990), 551-558). No case of an entirely novel function has been documented.

>Recent outbreaks of tuberculosis have fostered new research into this
>disease. It has been demonstrated that due to a mutation, the bacterium
>causing TB is now resistant to isoniazid, the main drug used in treatment.
>Thanks to a hard-working research community, a genetic basis has been
>identified for TB drug resistance.

I am not familiar with this case.

>What has been recognized already at the level of the microbe can also be
>witnessed at the highest levels of life. Among human populations, skin
>color affects the absorption of vitamin D from sunlight. Higher latitudes
>have decreased sunlight, lighter skin improves absorption, and
>lighter-skinned peoples are found at higher latitudes.

Sunlight (ultraviolet) produces vitamins D from various cholesterol
derivatives present in the skin. Skin color depends on the amount of
specific ultraviolet-absorbing pigments synthesized in the skin, which
obviously is regulated differently in different so-called "races", and
the specific types of regulation are inherited. The differences must
have been produced by evolution from common ancestors after the origin
of modern humans. But there is no indication that the amount of
insolation produced these differences. Differential survival may be
sufficient. There is no indication for the production of a novel gene.

>Sickle cell anemia is a genetic disease affecting some black populations.
>This gene is recessive and appears to afford enhanced resistance to
malaria.
>The sickle cell trait may have been a genetic response to an environmental
>danger.
>
>There is an increased risk of inheriting the genetic disorder, Tay-Sachs
>syndrome, among Ashkenazi Jews, and this has been traced to Polish
ghettoes
>in World War II. Though, like sickle cell, the disease is fatal where one
>inherits the gene from both parents, yet the Tay-Sachs gene has been
>correlated to an increased resistance to tuberculosis, the scourge of the
>ghettoes in those days.

Sickle cell anemia and Tay-Sachs disease are two human cases paralleling
the streptomycin resistance in E.coli (see above): a lethal danger is
overcome by means of a lesser damage. Again, differential survival after
a simple damaging mutation. There is no need here of invoking
"constructive" evolution.

>Researchers have begun preliminary investigations in this general area of
>inheritance affected by environmental factors. A conference was held in
>Pittsburgh in September, 1992, on "male-mediated toxicity."
>
>After 3 days, the consensus was that there is an
>urgent need for studies to elucidate mechanisms
>underlying tantalizing evidence that many different
>types of paternal exposure induce changes in sperm
>or semen that could affect children's health.

As much more sperm is produced than oocytes, there is much more DNA
replication in sperm precursors than in oocyte precursors, with a
concomitantly increased number of mutations (cf. Ellegren H., "Human
mutation - blame (mostly) men", Nature Genetics 31 (2002), 9-10; Hurst
L.D., Ellegren H., "Mystery of the mutagenic male", Nature 420 (2002),
365-366).

>In the not too distant future we may discover how adaptive genetic
mutations
>may be shaped by environmental forces, something that was postulated an
>early pioneer of evolution theory, J. B. Lamarck.

Lamarck speculated that environmental influences may produce inheritable
adaptive changes specifically corresponding to the influence. With the
detection of the genetic basis of the phenotype, Lamarckism was out for
good. The "adaptive mutations" discussed more recently have nothing to
do with Lamarckism. I treated some examples above.

Peter

-- 
Dr. Peter Ruest, CH-3148 Lanzenhaeusern, Switzerland
<pruest@dplanet.ch> - Biochemistry - Creation and evolution
"..the work which God created to evolve it" (Genesis 2:3)