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Topic Name: Researchers Explan for Evolutionary Changes in Genetic Sex-Determination Systems
Category: Genetic Engineering
Research persons: Sander van Doorn,Mark Kirkpatrick
Location: Santa Fe Institute, United States
Details
In animals with separate sexes, embryos commit to becoming male or female at
an early stage. Often this key decision is made by sex
determination genes on the sex chromosomes.
The genes involved in sexual development have changed remarkably little during
evolution. In contrast, the sex determination genes and the sex chromosomes
themselves are among the most rapidly changing features of the genome.
A research team formed by Sander van Doorn (Santa
Fe Institute, USA) and Mark Kirkpatrick (University
of Texas at Austin, USA) suggests an answer to the puzzle of why sex
chromosomes evolve so rapidly. In a theoretical study published in the October
17, 2007 issue of NATURE they demonstrate that sexual
conflict can establish novel sex-determining genes and sex chromosomes. The
proposed mechanism extends the established theory on the origin of sex
chromosomes, and it explains how sex determination can move from an ancestral
sex chromosome to an autosome, a non-sex-chromosome, that then invades to become
a new sex chromosome.
The mechanism suggested by these authors begins with an autosome that carries
two genes with particular features. One of these two genes is under sexually
antagonistic selection. This means that some versions of the gene (alleles) are
more beneficial in males than in females, while other alleles are more
beneficial for females. The other gene influences the sex of the individual.
Natural selection produces an association between the two genes – an allele
that is most beneficial in males will occur most often with the allele of the
other gene that makes the individual male. It is then possible that this new
male-making, male-benefiting (or female-making, female-benefiting) combination
of genes spreads through the population, eventually replacing the old pair of
sex chromosomes.
Genes with sexually antagonistic fitness effects and mutations that influence
sex determination appear to be common in nature,
but how would we know if the model presented here actually caused a change in
the sex-determination mechanism in a particular species" One possible test
would look at sexually antagonistic genes on a chromosome immediately before and
after that chromosome took over the role of sex determination. This might be
possible by comparing closely related species with different sex chromosomes.
One species would have a very young set of sex chromosomes, while the other
would still use the old sex chromosomes, and might approximate the state of the
chromosome right before the switch.
About Researchers:
Sander van Doorn
Postdoctoral Fellow, Santa Fe Institute
Short Bio:
I am interested in the evolution of biological diversity and the origin of
new species. Natural selection (survival of the fittest) decreases genetic
diversity unless selection is frequency-dependent. Frequency-dependent selection
thus figures prominently in most theories of speciation. My research examines
how genetic systems respond to frequency-dependent selection. In constrained
genetic systems frequency-dependent disruptive selection can support genetic
diversity and, potentially, lead to speciation. Developmentally flexible genetic
systems could respond in alternative ways as well, e.g., by evolving the
capacity to express different phenotypes without underlying genetic
differentiation. Will such phenotypic plasticity undermine the potential for
speciation, or will it actually facilitate the process by predisposing
populations to evolve developmental incompatibilities, as has recently been
argued? To answer this question I aim to develop simulation models and
analytical tools to deal with phenotypic plasticity in evolutionary models.
Besides this project I work with various collaborators on a number of topics
relating to sexual selection: sex-chromosome evolution, mutual mate choice, and
the evolution of dual-utility signals in mate choice and mate competition.
Contact:
Email:
vandoorn@santafe.edu
SFI Info: phone
& office
Mark Kirkpatrick
Education:
- B.A., Magna cum Laude with highest honors, Biology,
Harvard University, 1978
- Ph.D., Zoology, University of Washington, 1983
Contact:
E-mail:
kirkp@mail.utexas.edu
Office:
PAT 652
(512) 471-5996
Lab:
PAT 648
(512) 471-3760
Fax:
(512) 471-3878
About Santa Fe Institute (SFI)
The Santa Fe Institute (SFI) is a non-profit research institute dedicated to
the study of complex systems in Santa Fe, New Mexico.
Overview
The Santa Fe Institute was founded in 1984 by George Cowan, David Pines,
Stirling Colgate, Murray Gell-Mann, Nick Metropolis, Herb Anderson, Peter A.
Carruthers, and Richard Slansky. All but Pines and Gell-Mann were scientists
with Los Alamos National Laboratory.
SFI's original mission was to disseminate the notion of a separate
interdisciplinary research area, complexity theory referred to at SFI as
"complexity science". Recently it has announced that its original
mission to develop and disseminate a general theory of complexity has been
realized. It noted that numerous complexity institutes and departments have
sprung up around the world:
the CCS and CSCS at the University of Michigan.
The CSE at UC Davis
and the NECSI),
And it noted that it was working on updating its mission for the coming fifty
years.
SFI's complexity research led to efforts to create artificial life modeling real
organisms and ecosystems in the 1980s and 1990s.
It is also mainly from the various works of the SFI that was founded the
complexity economics school of thought.
SFI is also coordinating the Evolution of Human Languages project, an attempt to
trace all human language to a common root.
The publications of the Santa Fe Institute Studies in the Sciences of Complexity
all carry an imprint inspired by a Mimbres pottery design.
 
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