Monoubiquitination-dependent chromatin loading of FancD2 in silkworms, a species lacking the FA core complex

研究成果: Contribution to journalArticle査読

8 被引用数 (Scopus)

抄録

The Fanconi anemia (FA) pathway is required for activation and operation of the DNA interstrand cross-link (ICL) repair pathway, although the precise mechanism of the FA pathway remains largely unknown. A critical step in the FA pathway is the monoubiquitination of FANCD2 catalyzed by a FA core complex. This modification appears to allow FANCD2 to coordinate ICL repair with other DNA repair proteins on chromatin. Silkworm, . Bombyx mori, lacks apparent homologues of the FA core complex. However, BmFancD2 and BmFancI, the putative substrates of the complex, and BmFancL, the putative catalytic E3 ubiquitin ligase, are conserved. Here, we report that the silkworm FancD2 is monoubiquitinated depending on FancI and FancL, and stabilized on chromatin, following MMC treatment. A substitution of BmFancD2 at lysine 519 to arginine abolishes the monoubiquitination, but not the interaction between the FancD2 and FancI. In addition, we demonstrated that depletion of BmFancD2, BmFancI or BmFancL had effects on cell proliferation in the presence of MMC. These results suggest that the FA pathway in . B. mori works in the same manner as that in vertebrates.

本文言語英語
ページ(範囲)180-187
ページ数8
ジャーナルGene
501
2
DOI
出版ステータス出版済み - 6 15 2012

All Science Journal Classification (ASJC) codes

  • 遺伝学

フィンガープリント

「Monoubiquitination-dependent chromatin loading of FancD2 in silkworms, a species lacking the FA core complex」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル