Steve writes:

> The article is incorrect when it states that the daughter will be
>  genetically identical to the mother. One of the key elements of the
>  meiosis process that produces gametes is the "crossing over" activity in
>  Prophase I, where the homologous chromosome pairs "mix up" the gene
>  sequences by swapping apparently-random pieces of themselves with each
>  other. As a result, each gamete (sperm or egg) is more-or-less
>  genetically unique, and all of them are different from the source.

Not having the slightest idea what the original topic of this thread was (but
not letting that stop me), Steve's paragraph isn't quite correct either.

What I normally write on this subject is some variation of the following
paragraphs. The following is from a paper I wrote in the IEEE TRANSACTIONS ON
NEURAL NETWORKS, VOL. 5, NO. 1, JANUARY, 1994. pp. 130-148:
:

======================================

A. The Biological Role and Function of Crossing Over.

Because of the current emphasis placed on crossing over within genetic
algorithm research, a review of the biological function and purpose of
crossing over, as it is currently understood, is warranted. In distinct
contrast to inter-organismal chromosomal recombination (sex), crossing over
is a cell-internal intranuclear process that appears to be under active
promotion by the processes that regulate meiotic nuclear division.

If every gene were encoded as an independent chromosome, crossing over would
be unneccessary. But, in mammals, ca. 4000 gene functions reside on a single
chromosome. Otherwise fit alleles potentially suffer the deleterious
consequences of being physically linked with a severe defect resident
anywhere on a chromosome. Crossing over would seem to offer the possibility
of breaking such linkage disequilibria, informationally separating fit
alleles from the accidental consequences of physically residing near a
defect.

The phenomenon of crossing over was discovered during the period 1908-1915 by
Thomas Hunt Morgan and his students. The discovery that genes could cross
between chromosomes came as a great shock, similar to the excitement Barbara
McClintock's discovery of transposable elements ("jumping genes") created
during the 1970s. "As Muller [48] has characterized it...'the fact that
Morgan's evidence for [genes] crossing over [from one chromosome to the
other] and his suggestion that genes further apart cross over more frequently
was a thunderclap, hardly second to the discovery of Mendelism'" ([5] p.
753). In the 80 years since, however, the value and role of crossing over has
been steadily devalued from its earlier presumed importance as a fundamental
evolutionary process.

Crossing over exists, but it is not necessary to the process of meiosis (the
redundancy-reduction step characteristic of cellular gametogenesis in sexual
species). Indeed, in Drosophila males, no potential for crossing over exists
because no chiasmata form ([27] pp. 146-154, [42]). (Chiasma are the visible
cytological events where two arms of homologous chromatids overlap.)

In the males of a great many species, the rates of allelic recombination
(synonymous with an early definition of crossing over) is either much reduced
or altogether absent. In Lepidoptera (butterflies, moths, skippers) however,
the situation is reversed, as was first discovered by Sturtevant in 1915. He
found that female silkworms and wax moths do not undergo allelic
recombination because there is no formation of chiasmata, whereas males do
form chiasmata. In Diptera (flies), males are heterogametic; they possess one
pair of unpaired (non-homologous) sex chromosomes. In contrast, in
Lepidoptera, females are heterogametic. What informational advantage this
sex-linked suppression of chiasma formation confers to the species is not
clear, but the reduction in the formation of chiasmata in the heterogametic
sex is probably not coincidental, but rather "programmed".

Neither is the advantage that crossing over, when it exists, offers the
species clear. Two recent contending hypotheses are those of Maynard Smith
[43] and Bernstein, Hopf, and Michod [44]. Maynard Smith argues a role and
purpose for crossover not unlike sex itself. In this view, crossing over acts
a mutagenesis accelerator by increasing the rate of allelic recombination, in
effect, a kind of sex on top of sex. In contrast, Bernstein et al., who argue
a DNA repair role for crossing over, also argue that the rates of crossing
over are insufficient to maintain the accelerator of adapation that Maynard
Smith proposes. "The fraction of physical recombination events [the formation
of visible chiasmata] that result in allelic recombination is infinitesimally
small...The fraction of total recombination events that result in [actual]
allelic exchange at meiosis is...less than 2.6 x 10-6" [44].

These points can be agreed upon: (i) chiasmata form during meiosis and, in
some species, during mitosis, (ii) the rates of chiasmata formation are not
synonymous with the rates of allelic recombination, (iii) the process almost
certainly has some -- but currently unclear -- evolutionary purpose.

The principal argument supporting the last statement is the general
recognition that crossing over is a "promoted" process rather than an
uncorrected, persistent expression of residual error. The evidence for the
active intranuclear promotion of crossing over is two-fold: (i) proteins with
strand exchange activity have now been identified in organisms as diverse as
the bacteriophage T4 (a virus), bacteria, lower eukaryotes, and human cells.
This commonality implies that DNA strand exchange is a property of a
ubiquitous class of proteins that can be referred to as recombinases ([45]
and references therein). And, (ii) the crossing-over process must be presumed
to be under active promotion because it can be so easily suppressed in one
sex or the other. Only an actively coded process can be easily suppressed. A
random error process cannot likely be subject to easy sex-specific
suppression. If it were, and if the process had no positive evolutionary
value, it would quickly disappear in both sexes.

It is however also possible to argue with some lesser force of logic that
current evidence suggests no evolutionary role for crossing over. It is
simply a cytological process that results in no significant genomic
alterations. In human females, the rate of chiasma formation is 1.89 per
bivalent. If the rate of allelic recombination is as low as Bernstein et al.
calculate, the process is insignificant in its effects when compared to
sexually-mediated chromosomal recombination. DNA cannot be broken at any
arbitrary point. The mechanism that allows true allelic recombination to
occur at all is perhaps no more complicated than the majority of the DNA on a
chromosome is pseudogenetic and no longer actively translated. Breaking such
structure is quite likely to be often informationally neutral, and thus
tolerable.

Among the more intriguing aspects of crossing over is that it is almost
always differentially expressed in the two sexes, and in that, shares broad
characteristics with a number of other genetical phenomena. Haplodiploidy is
a sex-differentiated phenomenon that differentially exposes defects in the
male genome to direct selection. Under haplodiploidy, males are haploid and
thus practical allelic recombination during meiosis is functionally
impossible. Parahaploidy is a directly related condition that has been found
to exist in some mites. In this condition, male and female zygotes are fully
diploid, but the male sheds his paternal genome sometime prior to sexual
maturation, and thus allelic recombination in the male is again impossible.
In all placental mammals, the rate of chiasma formation during meiosis is ca.
30% higher in the female than the male. Achiasmatic meiosis is the rule in
most insects which are male heterogametic. The sum of these phenomena suggest
that crossing over serves an informational maintenance purpose rather than
act as the accelerator of adaptation that Maynard Smith has suggested.

=======================================

Clear as mud, eh?

The bottom line is that chiasmata don't form in every prophase (in fact, in
some species and especially some genders of those species, they don't form at
all), and therefore the genetical process of "crossing-over" doesn't occur.
In those circumstances, the nuclear complements of the formed gametes are
identical to their parental constituents, at least as a haploid subset of the
diploid parent.

Wirt Atmar

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