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

doi:10.1016/j.febslet.2014.09.009

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

Agricultural Bioresource Sciences

Research output: Contribution to journal › Article › peer-review

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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 language	English
Pages (from-to)	3959-3963
Number of pages	5
Journal	FEBS Letters
Volume	588
Issue number	21
DOIs	https://doi.org/10.1016/j.febslet.2014.09.009
Publication status	Published - Nov 3 2014

All Science Journal Classification (ASJC) codes

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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

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.",

author = "Ryohei Sugahara and Hiroaki Mon and Lee, {Jae Man} and Takahiro Shiotsuki and Takahiro Kusakabe",

note = "Funding Information: This work was supported in part by KAKENHI No. 26252057 from the Japan Society for the Promotion of Science. Publisher Copyright: {\textcopyright} 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.",

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doi = "10.1016/j.febslet.2014.09.009",

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T1 - Differential contribution of the Fanconi anemia-related proteins to repair of several types of DNA damage in cultured silkworm cells

AU - Sugahara, Ryohei

AU - Mon, Hiroaki

AU - Lee, Jae Man

AU - Shiotsuki, Takahiro

AU - Kusakabe, Takahiro

N1 - Funding Information: This work was supported in part by KAKENHI No. 26252057 from the Japan Society for the Promotion of Science. Publisher Copyright: © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

PY - 2014/11/3

Y1 - 2014/11/3

N2 - 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.

AB - 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.

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ER -

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

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