RT Journal Article
SR Electronic
T1 GA-repeats on mammalian X chromosomes support Ohno’s hypothesis of dosage compensation by transcriptional upregulation
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 485300
DO 10.1101/485300
A1 Edridge D’Souza
A1 Elizaveta Hosage
A1 Kathryn Weinand
A1 Steve Gisselbrecht
A1 Vicky Markstein
A1 Peter Markstein
A1 Martha L. Bulyk
A1 Michele Markstein
YR 2018
UL http://biorxiv.org/content/early/2018/12/04/485300.abstract
AB Over 50 years ago, Susumo Ohno proposed that dosage compensation in mammals would require upregulation of gene expression on the single active X chromosome, a mechanism which to date is best understood in the fruit fly Drosophila melanogaster. Here, we report that the GA-repeat sequences that recruit the conserved MSL dosage compensation complex to the Drosophila X chromosome are also enriched across mammalian X chromosomes, providing genomic support for the Ohno hypothesis. We show that mammalian GA-repeats derive in part from transposable elements, suggesting a mechanism whereby unrelated X chromosomes from dipterans to mammals accumulate binding sites for the MSL dosage compensation complex through convergent evolution, driven by their propensity to accumulate transposable elements.