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Resources » Paper

Kramer M et al. (2016) Genetics "Sex-Biased Expression of the Caenorhabditis elegans X Chromosome Is a result of Both X Chromosome Copy Number and Sex-Specific Gene Regulation."

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  • Comments on Kramer M et al. (2016) Genetics "Sex-Biased Expression of the Caenorhabditis elegans X Chromosome Is a result of Both X Chromosome Copy Number and Sex-Specific Gene Regulation." (0)

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    PMID:
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    Publication type:
    Journal_article
    WormBase ID:
    WBPaper00049769

    Kramer M, Rao P, & Ercan S (2016). Sex-Biased Expression of the Caenorhabditis elegans X Chromosome Is a result of Both X Chromosome Copy Number and Sex-Specific Gene Regulation. Genetics. doi:10.1534/genetics.116.190298

    Dosage compensation mechanisms equalize the level of X chromosome expression between sexes. Yet the X chromosome is often enriched for genes exhibiting sex-biased, i.e. imbalanced expression. The relationship between X chromosome dosage compensation and sex-biased gene expression remains largely unexplored. Most studies determine sex biased gene expression without distinguishing between contributions from X chromosome copy number (dose) and the animal's sex. Here, we uncoupled X chromosome dose from sex-specific gene regulation in C. elegans to determine the effect of each on X expression. In early embryogenesis, when dosage compensation is not yet fully active, X chromosome dose drives the hermaphrodite-biased expression of many X-linked genes, including several genes that were shown to be responsible for hermaphrodite fate. A similar effect is seen in the C. elegans germline, where X chromosome dose contributes to higher hermaphrodite X expression, suggesting that lack of dosage compensation in the germline may have a role in supporting higher expression of X chromosomal genes with female-biased functions in the gonad. In the soma, dosage compensation effectively balances X expression between the sexes. As a result, somatic sex-biased expression is almost entirely due to sex-specific gene regulation. These results suggest that lack of dosage compensation in different tissues and developmental stages allow X chromosome copy number to contribute to sex-biased gene expression and function.


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