comments: Sex and speciation: species group selection?
I would like to make the following comment on the 360 bp satellite 
repeat from D. melanogaster which I have reported two years ago 
(Advances in Genetics, vol 58, p.7). As I emphasized in recent 
comments to Flybase, this sequence is present at many X linked sites, 
including some near the 3' end of rox1 (involved in dosage 
compensation of X linked genes), the 5' and 3' ends of Hmr (involved 
in speciation) and its closely linked gene Rab9D that has five 
neighbouring paralogs (RabX2, Rab9Db, Rab9E, Rab9Fa and Rab9Fb). I 
recently observed that the repeat is also present at the Dox and Nmy 
genes from D. simulans and D. mauritiana, which are involved in sex 
ratio meiotic drive. Taken together, these observations make me 
speculate on the possibility that the above repeat, present on the X 
chromosome of all species of the melanogaster subgroup species, might 
confer a selective advantage at the species group level by promoting 
speciation.
In sharp contrast with genomes from parthenogenetic species 
(bound to go extinct) that have a limited lifespan on an evolutionary 
time scale, genomes of sexually reproducing species can survive for 
considerable periods of time through multiple speciation events. With 
regard to this, genetic factors that can influence both the evolution 
of sex through loss of genetic recombination (achiasmatic meiosis) and 
differentiation of sex chromosomes (a process somehow related to 
dosage compensation of X linked genes and control of sex ratio), might 
become most wanted candidates for speciation. Indeed, the above sex 
related characteristics share a capacity for generating intra- and 
intergenomic conflicts, potentially resulting in genetic 
incompatibilities between members of a population. In this view, 
additive effects of the above features underlying the evolution of sex 
may recurrently pave the way for speciation. The above 360 bp 
satellite repeat appears to be such a candidate for promoting genetic 
incompatibilities, for instance through 
modification of chromatin regulation. As I pointed out before, the 
repeat appears to be transcribed at least in embryos from the CG34339- 
RB (CG42611-RB) gene, suggesting a mechanism of regulation by RNA interference.
Pierre Hutter, PhD, FAMH
Chef de l'Unité de Génétique Médicale
Institut Central des Hôpitaux Valaisans
Av. Grand-Champsec 86
1951 Sion, Switzerland