Journal
DEVELOPMENTAL BIOLOGY
Volume 286, Issue 2, Pages 587-600Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2005.07.030
Keywords
non-coding RNA; imprinting; Prader-Willi; Angelman; Ube3a; Snrpn
Categories
Funding
- NCI NIH HHS [R01 CA79716, R01 CA75389, R01 CA099471] Funding Source: Medline
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The mouse ortholog of the Prader-Willi/Angelman syndrome imprinted domain contains several paternal-specific transcripts and the maternally expressed gene encoding ubiquitin protein ligase E3A (Ube3a). A Large paternal Non-Coding RNA, encompassing Snurf-Snrpn exons and the Ube3a Antisense Transcript (Ube3a-ATS), has been recently characterized and named here LNCAT Potential roles of LNCAT in imprinting, gene regulation, and disease are likely but have not been investigated. In order to establish the function(s) of LNCAT, we first determined its in vivo spatio-temporal expression pattern at the cellular level during development and in different adult brain tissues. We show here that LNCAT is developmentally regulated, with transcript variants being specifically expressed through neuronal differentiation in postmitotic neurons. We demonstrate that the LNCAT and Snurf-Snrpn transcripts are independent although they share common exons. We show an absence of expression of LNCAT through gametogenesis and in early embryo excluding a role of LNCAT in the imprint establishment. We also report a range of observations that challenges the widely accepted model of imprinted gene silencing of Ube3a. Although these last data do not completely exclude that the LNCAT variants including Ube3a-ATS exons could repress the paternal allele of Ube3a, they do allow us to propose an alternative and consistent model. (C) 2005 Elsevier Inc. All rights reserved.
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