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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.