S.A.Thomsen <
s_a_t...@yahoo.com> wrote:
> Det har da inget med let/svært at gøre. Dem der gjorde det overlevede, dem
> der ikke gjorde det blev ædt. Simpel "Darvin udvælgelse".
En lille mutation forekommer så hyppigere end et utal af store.
> PS: At homosexualitet skulle være genetisk bestemt, er noget nonsens.
Måske skulle du så lige læse dette link fra Nature (11. januar 2007)
igen:
<
http://www.tiem.utk.edu/~gavrila/PAPS/Savolainen_Lehmann.pdf>
EVOLUTIONARY BIOLOGY
Genetics and bisexuality
Vincent Savolainen and Laurent Lehmann
A population-genetic model indicates that if there is a gene responsible
for homosexual behaviour it can readily spread in populations. The model
also predicts widespread bisexuality in humans.
For human societies at large, homosexuality is a sensitive issue. For
biologists it is an intriguing one1,2. How can genes influencing
homosexual — and so non-reproductive — behaviour be favoured by natural
selection? An answer is offered by Gavrilets and Rice in a paper that
has just appeared in Proceedings of the Royal Society3. They provide a
population-genetic analysis that explains why, in theory, a gene pre-
disposing an individual to homosexual behav- iour would spread in a
population, and that predicts its widespread occurrence in humans and
other sexually reproducing species.
No predisposing gene for homosexual behaviour has been identified, but
there is evidence that genetic controls are involved: for example, human
twins are more likely both to be gay compared with non-identical
brothers; and male homosexuality is more often inherited maternally,
indicating that heritable maternal effects and/or genes linked to the X
chromo- some are in operation. However, unlike heterosexuals, who devote
a significant amount of time to reproductive sex, homosexuals are
involved in non-reproductive sex, hampering the direct transmission of
any gene underlying this behaviour. Homosexuality has a cost to fit-
ness — that is, the ability of an individual to produce offspring that
survive and reproduce — and it can only evolve if it otherwise provides
indirect benefits to reproduction.
Three main mechanisms have been proposed in which variety in genes
controlling homosexuality could be maintained in a population:
overdominance, sexually antagonistic selection, and kin altruism. For
simplification, we will consider here male homosexuality, but these
mechanisms also apply to female homosexuality. They also apply no matter
how many genes contribute, but Gavrilets and Rice's analysis deals with
a single theoretical gene and its two variants (alleles).
First, in the case of overdominance, a 'gay allele' would result in
homosexual behaviour in an individual who has received this allele from
both parents (homozygous), but would provide an advantage to the
heterozygote (where only one parent has transmitted the gay allele).
This situation would be similar to the renowned example of sickle-cell
anaemia in Africa, a genetically inherited disease controlled by a
deficient allele. Homozygotes for this allele suffer severe disorders.
But because this allele con- fers resistance to malaria when
heterozygous, it is maintained in human populations exposed to malaria.
Under this scenario, heterozygotes for the gay allele may have higher
success in attracting females and/or their sperm may have some
competitive advantage.
In the second case, sexually antagonistic selection, a gay allele would
result in a cost when expressed in males ('feminization' and loss of
fitness), which would be counterbalanced by a fitness advantage when it
is expressed in females.
In the third hypothesis, kin altruism, homosexuals would help their own
family members, increasing the fitness of their relatives and therefore
the probability that a gay allele is passed on to the next generation.
These hypotheses have previously been speculative, but they have now
been modelled and formalized by Gavrilets and Rice. The authors adapted
the classical population-genetic equations established by J. B. S.
Haldane and describe the evolution of the frequency of two alleles at
one locus, in large populations for which each allele may result in
sex-specific effects on fitness. Considering hypothetical straight and
gay alleles, Gavrilets and Rice document the conditions of relative
costs and benefits to fitness under which the gay allele can enter a
population of straight alleles and be maintained subsequently. They
establish the conditions under both the overdominance and sexually
antagonistic-selection hypotheses for a homosexual gene that would be
located on autosomes (non-sexual chromosomes) or on the X chromosome.
These conditions still remain to be evaluated in the kin-altruism
hypothesis.
Crucially, in these population-genetic mod- els, a gay allele will
produce variable degrees of homosexual behaviour, which is equivalent to
the fitness cost of that behaviour (which, for example, could be
interpreted as the propor- tion of time devoted to homosexual rather
than reproductive sex). If one homozygous individual is not at all
involved in reproductive sex, then the cost of homosexuality is maximal
and this individual's phenotype is obviously strictly gay; however, in
all other combinations, homozygous individuals exhibit a degree of
bisexual behaviour depending on the costs.
Gavrilets and Rice show that, for a large set of costs and benefits, the
gay allele can invade a population. Under overdominance, once a gay
allele has entered a population it will be maintained in a polymorphic
equilibrium, and this is easier if the homosexual gene is autosomal
rather than X-linked. Further, under sexually antagonistic selection,
the gay allele may even go to fixation — that is, each individual will
become homozygous for this allele — thus implying widespread
bisexuality.
This theoretical framework is an advance in evolutionary biology and
studies of human behaviour because it generates several testable
predictions: for example, if a gene influencing homosexuality is linked
to the X chromosome, then it would support the sexual-antagonism
hypothesis rather than overdominance. The framework will be used to
guide research on the genetic basis of male and female homosexuality,
and will help in resolving the 'Darwinian paradox of male
homosexuality'. But it is of course theory only. Tasks for the future
are to establish more precisely the costs and benefits of such behaviour
in natural populations1. Such knowledge will help fine-tune these models
of sexual orientation and show whether overdominance or antagonistic
selection has been operating in mammals and throughout human history.
Vincent Savolainen is at the Jodrell Laboratory, Royal Botanic Gardens,
Kew, Richmond TW9 3DS, UK.
Laurent Lehmann is in the Department of Genetics, University of
Cambridge, Cambridge CB2 3HE, UK. e-mails:
v.savo...@kew.org;
l.le...@gen.cam.ac.uk
1. Bagemihl, B. Biological Exuberance: Animal Homosexuality and Natural
Diversity (St Martin's Press, New York, 1999).
2. Camperio-Ciani, A., Corna, F. & Capiluppi, C. Proc. R. Soc.
Lond. B 271, 2217–2221 (2004).
3. Gavrilets, S. & Rice, W. R. Proc. R. Soc. Lond. B 273,
3031–3038 (2006).
4. Wilson,E.O.Sociobiology:The New Synthesis(Harvard
Univ. Press, 1975).
5. MacIntyre, F. & Estep, K. W. Biosystems 31, 223–233
(1993).
6. Haldane,J.B.S.Trans.Camb.Phil.Soc.23,19–41(1924).
7. Karlin, S. Am. Math. Mon. 79, 699–739 (1972).
===
Se i øvrigt følgende dansk-sprogede artikel:
<
http://videnskab.dk/kort-nyt/homoseksualitet-hjalp-maske-vores-forfaedre-til-knytte-band>
Og lidt om årsagerne til homofobi:
<
http://www.pbs.org/wgbh/pages/frontline/shows/assault/roots/freud.html>
... frygt for den homoseksuelle side i én selv ...