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Title: Genome-wide RNAi screen identify melanoma-associated antigen Mageb3 involved in X chromosome inactivation
Authors: Li, Wei
Hong, Ru
Lai, Lan-Tian
Dong, Qiman
Ni, Peiling
Chelliah, Rosi
Huq, Mehnaz
Siti Nadirah Ismail
Chandola, Udita
Ang, Zhiwei
Lin, Bingqing
Chen, Xin
Chen, Lingyi
Zhang, Li-Feng
Keywords: Science::Biological sciences
Issue Date: 2018
Source: Li, W., Hong, R., Lai, L.-T., Dong, Q., Ni, P., Chelliah, R., . . . Zhang, L.-F. (2018). Genome-wide RNAi screen identify melanoma-associated antigen Mageb3 involved in X chromosome inactivation. Journal of Molecular Biology, 430(17), 2734-2746. doi:10.1016/j.jmb.2018.05.031
Journal: Journal of Molecular Biology
Abstract: Xist (inactivated X chromosome specific transcript) is a prototype long noncoding RNA in charge of epigenetic silencing of one X chromosome in each female cell in mammals. In a genetic screen, we identify Mageb3 and its homologs Mageb1 and Mageb2 as genes functionally required for Xist-mediated gene silencing. Mageb1–3 are previously uncharacterized genes belonging to the MAGE (melanoma-associated antigen) gene family. Mageb1–3 are expressed in undifferentiated ES cells and early stages of in vitro differentiation, a critical time window of X chromosome inactivation. Mageb3 showed both cytoplasmic and nuclear localization without enrichment on the inactive X (Xi). Mageb3 interacted with Polycomb group ring finger 3 (Pcgf3), a RING finger protein involved in recruiting Polycomb activities onto Xi. Mageb3 overexpression stabilized Pcgf3 protein. Mageb1–3 gene knockout affected H3K27me3 enrichment and the spreading of gene silencing along Xi. These data suggested that Mageb3 might regulate the recruitment of the Polycomb complex onto Xi and subsequent H3K27me3 modification through Pcgf3. Moreover, the nucleolar enrichment of Mageb3 was diminished when nuclear matrix factor hnRNP U is overexpressed, implying the interaction between Mageb3 and nuclear matrix, which is another possible mechanism for Mageb3 to regulate X chromosome inactivation.
ISSN: 0022-2836
DOI: 10.1016/j.jmb.2018.05.031
Rights: © 2018 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SPMS Journal Articles

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