Differentiation-dependent requirement of Tsix long non-coding RNA in imprinted X-chromosome inactivation

Emily Maclary, Emily Buttigieg, Michael Hinten, Srimonta Gayen, Clair Harris, Mrinal Kumar Sarkar, Sonya Purushothaman and Sundeep Kalantry ()
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Emily Maclary: University of Michigan Medical School
Emily Buttigieg: University of Michigan Medical School
Michael Hinten: University of Michigan Medical School
Srimonta Gayen: University of Michigan Medical School
Clair Harris: University of Michigan Medical School
Mrinal Kumar Sarkar: University of Michigan Medical School
Sonya Purushothaman: Brody School of Medicine, East Carolina University
Sundeep Kalantry: University of Michigan Medical School

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract Imprinted X-inactivation is a paradigm of mammalian transgenerational epigenetic regulation resulting in silencing of genes on the paternally inherited X-chromosome. The preprogrammed fate of the X-chromosomes is thought to be controlled in cis by the parent-of-origin-specific expression of two opposing long non-coding RNAs, Tsix and Xist, in mice. Exclusive expression of Tsix from the maternal-X has implicated it as the instrument through which the maternal germline prevents inactivation of the maternal-X in the offspring. Here, we show that Tsix is dispensable for inhibiting Xist and X-inactivation in the early embryo and in cultured stem cells of extra-embryonic lineages. Tsix is instead required to prevent Xist expression as trophectodermal progenitor cells differentiate. Despite induction of wild-type Xist RNA and accumulation of histone H3-K27me3, many Tsix-mutant X-chromosomes fail to undergo ectopic X-inactivation. We propose a novel model of lncRNA function in imprinted X-inactivation that may also apply to other genomically imprinted loci.

Date: 2014
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DOI: 10.1038/ncomms5209

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