Differential contribution of the Fanconi anemia-related proteins to repair of several types of DNA damage in cultured silkworm cells

Ryohei Sugahara, Hiroaki Mon, Jae Man Lee, Takahiro Shiotsuki, Takahiro Kusakabe

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

The silkworm Fanconi anemia (FA) pathway is required for normal cellular resistance to mitomycin C (MMC) in silkworms, but little is known about the requirement for repair of other types of DNA damage. Here we report that silkworm cells deficient for FA proteins FancD2 and FancM exhibit normal sensitivities to hydroxyurea (HU) and camptothecin (CPT), although FancM-dependent FancD2 monoubiquitination is induced upon these treatments. Similar results were observed in cells depleted for Rmi1 and Mhf1, which interact with the FancM protein. We also found that Rad51-knockdown cells exhibited normal sensitivity to HU despite induction of double-strand breaks by HU treatment.

Original languageEnglish
Pages (from-to)3959-3963
Number of pages5
JournalFEBS Letters
Volume588
Issue number21
DOIs
Publication statusPublished - Nov 3 2014

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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