Over the past decade, many studies documented high genetic divergence between closely related species in genomic regions experiencing restricted recombination in hybrids, such as within chromosomal rearrangements or areas adjacent to centromeres. Such regions have been called 'islands of speciation' because of their presumed role in maintaining the integrity of species despite gene flow elsewhere in the genome. Here, we review alternative explanations for such patterns. Segregation of ancestral variation or artifacts of nucleotide diversity within species can readily lead to higher F ST in regions of restricted recombination than other parts of the genome, even in the complete absence of interspecies gene flow, and thereby cause investigators to erroneously conclude that islands of speciation exist. We conclude by discussing strengths and weaknesses of various means for testing the role of restricted recombination in maintaining species.

Regional rates of recombination often correlate with levels of nucleotide diversity, and either selective or neutral hypotheses can explain this relationship. Regional recombination rates also correlate with nucleotide differences between human and chimpanzee, consistent with models where recombination is mutagenic; however, a lack of correlation is observed in the Drosophila melanogaster group, consistent with models invoking natural selection. Here, we revisit the relationship among recombination, diversity, and interspecies difference by generating empirical estimates of these parameters in Drosophila pseudoobscura. To measure recombination rate, we genotyped 1,294 backcross hybrids at 50 markers across the largest assembled linkage group in this species. Genome-wide diversity was estimated by sequencing a second isolate of D. pseudoobscura at shallow coverage. Alignment to the sequenced genome of the closely related species, Drosophila persimilis, provided nucleotide site orthology. Our findings demonstrate that scale is critical in determining correlates to recombination rate: fine-scale cross-over rate estimates are far stronger predictors of both diversity and interspecies difference than broadscale estimates. The correlation of fine-scale recombination rate to diversity and interspecies difference appears to be genome-wide, evidenced by examination of an X-linked region in greater detail. Because we observe a strong correlation of cross-over rate with interspecies difference, even after correcting for segregating ancestral variation, we suggest that both mutagenic and selective forces generate these correlations, the latter in regions of low crossing over. We propose that it is not cross-overs per se that are mutagenic, but rather repair of DNA double-strand break precursors via crossing over and gene conversion.variation ͉ crossing over O ne of the most influential observations in molecular evolutionary biology is the relationship between recombination rate and nucleotide diversity within species. In a pioneering study, Begun and Aquadro (1) identified a strong positive association between nucleotide polymorphism in Drosophila melanogaster (as measured from restriction site data of 20 loci) and recombination rate. If this relationship was caused by recombination itself being mutagenic, a similar relationship between recombination rate and nucleotide divergence to the sister species, Drosophila simulans, should also exist; however, this relationship was not observed. More recently, Begun et al.(2) examined whole-genome shotgun sequences from multiple strains of D. simulans and the published D. melanogaster genome assembly and confirmed these initial observations at an unprecedented scale. The association between recombination rate and diversity, but not divergence, in Drosophila is considered to be driven primarily by natural selection (3-5): fixation of positively selected variants and associated hitchhiking effects (6) and/or background selection eliminating deleterious alleles (7).Similar studies in o...

Prodigiosin: Amido‐functionalised prodigiosin‐derived compounds were synthesised via a robust and efficient synthetic route. These compounds were then evaluated against 60 human cell lines consisting of nine diverse tumour cell types and their anticancer activities were assessed.magnified image

The human cancer susceptibility gene, BRCA2, functions in double-strand break repair by homologous recombination, and it appears to function via interaction of a repetitive region ("BRC repeats") with RAD-51. A putatively simpler homolog, dmbrca2, was identified in Drosophila melanogaster recently and also affects mitotic and meiotic double-strand break repair. In this study, we examined patterns of repeat variation both within Drosophila pseudoobscura and among available Drosophila genome sequences. We identified extensive variation within and among closely related Drosophila species in BRC repeat number, to the extent that variation within this genus recapitulates the extent of variation found across the entire animal kingdom. We describe patterns of evolution across species by documenting recent repeat expansions (sometimes in tandem arrays) and homogenizations within available genome sequences. Overall, we have documented patterns and modes of evolution in a new model system of a gene which is important to human health.

The Bateson-Dobzhansky-Muller model posits that hybrid incompatibilities result from genetic changes that accumulate during population divergence. Indeed, much effort in recent years has been devoted to identifying genes associated with hybrid incompatibilities, often with limited success, suggesting that hybrid sterility and inviability are frequently caused by complex interactions between multiple loci and not by single or a small number of gene pairs. Our previous study showed that the nature of epistasis between sterility-conferring QTL in the Drosophila persimilis-D. pseudoobscura bogotana species pair is highly specific. Here, we further dissect one of the three QTL underlying hybrid male sterility between these species and provide evidence for multiple factors within this QTL. This result indicates that the number of loci thought to contribute to hybrid dysfunction may have been underestimated, and we discuss how linkage and complex epistasis may be characteristic of the genetics of hybrid incompatibilities. We further pinpoint the location of one locus that confers hybrid male sterility when homozygous, dubbed “mule-like”, to roughly 250 kilobases.