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Sex bias and dosage compensation in the zebra finch versus chicken genomes: General and specialized patterns among birds

    • 1 Department of Integrative Biology and Physiology and Laboratory of Neuroendocrinology of the Brain Research Institute, University of California, Los Angeles, California 90095-1606, USA;
    • 2 Institute for Genomic Biology, University of Illinois, Urbana–Champaign, Urbana, Illinois 61801, USA;
    • 3 Departments of Psychology and Zoology, Neuroscience Program, Michigan State University, East Lansing, Michigan 48824, USA
Published March 31, 2010. Vol 20 Issue 4, pp. 512-518. https://doi.org/10.1101/gr.102343.109
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cover of Genome Research Vol 36 Issue 4
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Abstract

We compared global patterns of gene expression between two bird species, the chicken and zebra finch, with regard to sex bias of autosomal versus Z chromosome genes, dosage compensation, and evolution of sex bias. Both species appear to lack a Z chromosome–wide mechanism of dosage compensation, because both have a similar pattern of significantly higher expression of Z genes in males relative to females. Unlike the chicken Z chromosome, which has female-specific expression of the noncoding RNA MHM (male hypermethylated) and acetylation of histone 4 lysine 16 (H4K16) near MHM, the zebra finch Z chromosome appears to lack the MHM sequence and acetylation of H4K16. The zebra finch also does not show the reduced male-to-female (M:F) ratio of gene expression near MHM similar to that found in the chicken. Although the M:F ratios of Z chromosome gene expression are similar across tissues and ages within each species, they differ between the two species. Z genes showing the greatest species difference in M:F ratio were concentrated near the MHM region of the chicken Z chromosome. This study shows that the zebra finch differs from the chicken because it lacks a specialized region of greater dosage compensation along the Z chromosome, and shows other differences in sex bias. These patterns suggest that different avian taxa may have evolved specific compensatory mechanisms.

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