HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
理学院・理学研究院  >
雑誌発表論文等  >

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

この資料はクリエイティブ・コモンズ・ライセンスの下で公開されています。

フルテキスト
Tange_et_al-2016-Genes_to_Cells.pdf2.28 MBPDF見る/開く
この文献へのリンクには次のURLを使用してください:http://hdl.handle.net/2115/62872

タイトル: Inner nuclear membrane protein Lem2 augments heterochromatin formation in response to nutritional conditions
著者: Tange, Yoshie 著作を一覧する
Chikashige, Yuji 著作を一覧する
Takahata, Shinya 著作を一覧する
Kawakami, Kei 著作を一覧する
Higashi, Masato 著作を一覧する
Mori, Chie 著作を一覧する
Kojidani, Tomoko 著作を一覧する
Hirano, Yasuhiro 著作を一覧する
Asakawa, Haruhiko 著作を一覧する
Murakami, Yota 著作を一覧する
Haraguchi, Tokuko 著作を一覧する
Hiraoka, Yasushi 著作を一覧する
発行日: 2016年 8月
出版者: Wiley-Blackwell
誌名: Genes to cells
巻: 21
号: 8
開始ページ: 812
終了ページ: 832
出版社 DOI: 10.1111/gtc.12385
抄録: 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.
資料タイプ: article
URI: http://hdl.handle.net/2115/62872
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 村上 洋太

 

本サイトに関するご意見・お問い合わせは repo at lib.hokudai.ac.jp へお願いします。 - 北海道大学