Summary: | <p>Abstract</p> <p>Background</p> <p>Paucity of male-biased genes on the <it>Drosophila X </it>chromosome is a well-established phenomenon, thought to be specifically linked to the role of these genes in reproduction and/or their expression in the meiotic male germline. In particular, meiotic sex chromosome inactivation (MSCI) has been widely considered a driving force behind depletion of spermatocyte-biased <it>X</it>-linked genes in <it>Drosophila </it>by analogy with mammals, even though the existence of global MCSI in <it>Drosophila </it>has not been proven.</p> <p>Results</p> <p>Microarray-based study and qRT-PCR analyses show that the dynamics of gene expression during testis development are very similar between <it>X</it>-linked and autosomal genes, with both showing transcriptional activation concomitant with meiosis. However, the genes showing at least ten-fold expression bias toward testis are significantly underrepresented on the <it>X </it>chromosome. Intriguingly, the genes with similar expression bias toward tissues other than testis, even those not apparently associated with reproduction, are also strongly underrepresented on the <it>X</it>. Bioinformatics analysis shows that while tissue-specific genes often bind silencing-associated factors in embryonic and cultured cells, this trend is less prominent for the <it>X</it>-linked genes.</p> <p>Conclusions</p> <p>Our data show that the global meiotic inactivation of the <it>X </it>chromosome does not occur in <it>Drosophila</it>. Paucity of testis-biased genes on the <it>X </it>appears not to be linked to reproduction or germline-specific events, but rather reflects a general underrepresentation of tissue-biased genes on this chromosome. Our analyses suggest that the activation/repression switch mechanisms that probably orchestrate the highly-biased expression of tissue-specific genes are generally not efficient on the <it>X </it>chromosome. This effect, probably caused by dosage compensation counteracting repression of the <it>X</it>-linked genes, may be the cause of the exodus of highly tissue-biased genes to the autosomes.</p>
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