An Xist-activating antisense RNA required for X-chromosome inactivation

Mrinal K. Sarkar, Srimonta Gayen, Surinder Kumar, Emily Maclary, Emily Buttigieg, Michael Hinten, Archana Kumari, Clair Harris, Takashi Sado and Sundeep Kalantry ()
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Mrinal K. Sarkar: University of Michigan Medical School
Srimonta Gayen: University of Michigan Medical School
Surinder Kumar: University of Michigan Medical School
Emily Maclary: University of Michigan Medical School
Emily Buttigieg: University of Michigan Medical School
Michael Hinten: University of Michigan Medical School
Archana Kumari: University of Michigan Medical School
Clair Harris: University of Michigan Medical School
Takashi Sado: Graduate School of Agriculture, Kinki University
Sundeep Kalantry: University of Michigan Medical School

Nature Communications, 2015, vol. 6, issue 1, 1-13

Abstract: Abstract The transcriptional imbalance due to the difference in the number of X chromosomes between male and female mammals is remedied through X-chromosome inactivation, the epigenetic transcriptional silencing of one of the two X chromosomes in females. The X-linked Xist long non-coding RNA functions as an X inactivation master regulator; Xist is selectively upregulated from the prospective inactive X chromosome and is required in cis for X inactivation. Here we discover an Xist antisense long non-coding RNA, XistAR (Xist Activating RNA), which is encoded within exon 1 of the mouse Xist gene and is transcribed only from the inactive X chromosome. Selective truncation of XistAR, while sparing the overlapping Xist RNA, leads to a deficiency in Xist RNA expression in cis during the initiation of X inactivation. Thus, the Xist gene carries within its coding sequence an antisense RNA that drives Xist expression.

Date: 2015
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DOI: 10.1038/ncomms9564

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