Abstract
Y chromosomes play important roles in sex determination and male fertility. In several groups (e.g., mammals) there is strong evidence that they evolved through gene loss from a common X-Y ancestor, but in Drosophila the acquisition of new genes plays a major role. This conclusion came mostly from studies in two species. Here we report the identification of the 22 Y-linked genes in D. willistoni. They all fit the previously observed pattern of autosomal or X-linked testis-specific genes that duplicated to the Y. The ratio of gene gains to gene losses is ~25 in D. willistoni, confirming the prominent role of gene gains in the evolution of Drosophila Y chromosomes. We also found four large segmental duplications (ranging from 62 kb to 303 kb) from autosomal regions to the Y, containing ~58 genes. All but four of these duplicated genes became pseudogenes in the Y or disappeared. In the GK20609 gene the Y-linked copy remained functional, whereas its original autosomal copy degenerated, demonstrating how autosomal genes are transferred to the Y chromosome. Since the segmental duplication that carried GK20609 contained six other testis-specific genes, it seems that chance plays a significant role in the acquisition of new genes by the Drosophila Y chromosome.
Highlights
Y chromosomes nearly always contain male-fertility genes, and in many species carry the master sex-determining genes [1–4]
The last column, which shows the amount of sequence in the scaffolds, clarifies that the Y chromosome is relatively small; because it is a repeat-rich region, Y-linked sequences are prone to assembly fragmentation and tend to get scattered in numerous small scaffolds
If we adopt the cut-off of 60% unmatched sequences, we find that the Y-chromosome in the Sanger assembly contains 28.5 Mbp, whereas the X and autosomes amount to 189.8 Mbp; the corresponding values for the PacBio assembly are 49.4 Mbp and 197.6 Mbp
Summary
Y chromosomes nearly always contain male-fertility genes, and in many species carry the master sex-determining genes [1–4]. Further theoretical and empirical studies (reviewed in [7,8]) supported these initial suggestions
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