A requirement of FancL and FancD2 monoubiquitination in DNA repair

Sohsuke Seki, Mioko Ohzeki, Akiko Uchida, Seiki Hirano, Nobuko Matsushita, Hiroyuki Kitao, Tsukasa Oda, Takayuki Yamashita, Naoki Kashihara, Akio Tsubahara, Minoru Takata, Masamichi Ishiai

研究成果: Contribution to journalArticle査読

30 被引用数 (Scopus)

抄録

The rare hereditary disorder Fanconi anemia (FA) can be caused by mutations in components of the FA core complex (FancA/B/C/E/F/G/L/M), a key regulator FancD2, the breast cancer susceptibility protein BRCA2/ FancD1, or the newly identified FancJ/BRIP1 helicase. By performing yeast two-hybrid (Y2H) screens using N-terminal chicken (ch) FancD2 as a bait, we have identified chFancL, the likely ubiquitin E3 ligase subunit of the FA core complex. We also found that ectopically expressed FancD2 and FancL co-immunoprecipitated in 293T cells, and this interaction was dependent on the PHD domain of FancL. FANCL-disrupted chicken DT40 cells displayed defects in both FancD2 monoubiquitination and focus formation. Importantly, cell lines lacking the FANCL or FANCD2 genes, or carrying a "knock-in" mutation of the FancD2 monoubiquitination site (where the Lys 563 residue is changed to Arg), displayed quantitatively identical defects in the repair of I-SceI-induced chromosomal breaks by homologous recombination (HR). These data establish the role of FANCL and FancD2 monoubiquitination in HR repair.

本文言語英語
ページ(範囲)299-310
ページ数12
ジャーナルGenes to Cells
12
3
DOI
出版ステータス出版済み - 3 2007
外部発表はい

All Science Journal Classification (ASJC) codes

  • 遺伝学
  • 細胞生物学

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