Involvement of Matrin 3 and SFPQ/NONO in the DNA damage response

Maayan Salton, Yaniv Lerenthal, Shih Ya Wang, David J. Chen, Yosef Shiloh*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

159 Scopus citations


The DNA damage response (DDR) is a complex signaling network that is induced by DNA lesions and vigorously activated by double strand breaks (DSBs). the DSB response is mobilized by the nuclear protein kinase AtM, which phosphorylates key players in its various branches. SFpQ (pSF) and NoNo (p54) are nuclear proteins that interact with each other and have diverse roles in nucleic acids metabolism. the SFpQ/NoNo heterodimer was previously found to enhance DNA strand break rejoining in vitro. our attention was drawn to these two proteins as they interact with the nuclear matrix protein Matrin 3 (MAtR3), which we found to be a novel AtM target. We asked whether SFpQ and NoNo too are involved in the DSB response. proteins that function at the early phase of this response are often recruited to the damaged sites. We observed rapid recruitment of SFpQ/NoNo to sites of DNA damage induced by laser microbeam. In MAtR3 knockdown cells SFpQ/NoNo retention at DNA damage sites was prolonged. SFpQ and MAtR3 depletion led to abnormal accumulation of cells at the S-phase of the cell cycle following treatment with the radiomimetic chemical neocarzinostatin. Notably, proteins involved in DSB repair via nonhomologous end-joining co-immunoprecipitated with NoNo; SFpQ depletion delayed DSB repair. Collectively the data suggest that SFpQ, NoNo and MAtR3 are involved in the early stage of the DSB response, setting the scene for DSB repair.

Original languageAmerican English
Pages (from-to)1568-1576
Number of pages9
JournalCell Cycle
Issue number8
StatePublished - 15 Apr 2010
Externally publishedYes

Bibliographical note

Funding Information:
We thank Y. Shav-Tal for useful advice; Y. Ziv for helpful suggestions, M. Lavin for a lymphoblastoid cell line, and G. Patton, T. Halazonetis, S. Jackson and S. Burma for antibodies. This research was supported by research grants from the A-T Medical Research Foundation and the Israel Cancer Research Fund (to Y.S.) and the National Institutes of Health (CA050519 and CA13499 to D.J.C.). M. Salton is a Joseph Sassoon Fellow. Y. Shiloh is a Research Professor of the Israel Cancer Research Fund.


  • ATM
  • Cell cycle checkpoint
  • DNA damage response
  • Matrin 3
  • NONO/p54


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