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Inner nuclear membrane protein Lem2 augments heterochromatin formation in response to nutritional conditions

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Title: Inner nuclear membrane protein Lem2 augments heterochromatin formation in response to nutritional conditions
Authors: Tange, Yoshie Browse this author
Chikashige, Yuji Browse this author
Takahata, Shinya Browse this author
Kawakami, Kei Browse this author
Higashi, Masato Browse this author
Mori, Chie Browse this author
Kojidani, Tomoko Browse this author
Hirano, Yasuhiro Browse this author
Asakawa, Haruhiko Browse this author
Murakami, Yota Browse this author
Haraguchi, Tokuko Browse this author
Hiraoka, Yasushi Browse this author
Issue Date: Aug-2016
Publisher: Wiley-Blackwell
Journal Title: Genes to cells
Volume: 21
Issue: 8
Start Page: 812
End Page: 832
Publisher DOI: 10.1111/gtc.12385
PMID: 27334362
Abstract: Inner nuclear membrane proteins interact with chromosomes in the nucleus and are important for chromosome activity. Lem2 and Man1 are conserved members of the LEM-domain nuclear membrane protein family. Mutations of LEM-domain proteins are associated with laminopathy, but their cellular functions remain unclear. Here, we report that Lem2 maintains genome stability in the fission yeast Schizosaccharomyces pombe. S.pombe cells disrupted for the lem2(+) gene (lem2) showed slow growth and increased rate of the minichromosome loss. These phenotypes were prominent in the rich culture medium, but not in the minimum medium. Centromeric heterochromatin formation was augmented upon transfer to the rich medium in wild-type cells. This augmentation of heterochromatin formation was impaired in lem2 cells. Notably, lem2 cells occasionally exhibited spontaneous duplication of genome sequences flanked by the long-terminal repeats of retrotransposons. The resulting duplication of the lnp1(+) gene, which encodes an endoplasmic reticulum membrane protein, suppressed lem2 phenotypes, whereas the lem2 lnp1 double mutant showed a severe growth defect. A combination of mutations in Lem2 and Bqt4, which encodes a nuclear membrane protein that anchors telomeres to the nuclear membrane, caused synthetic lethality. These genetic interactions imply that Lem2 cooperates with the nuclear membrane protein network to regulate genome stability.
Type: article
Appears in Collections:理学院・理学研究院 (Graduate School of Science / Faculty of Science) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 村上 洋太

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