Identity and Function of a Large Gene Network Underlying Mutagenic Repair of DNA Breaks

Author:

Al Mamun Abu Amar M.1,Lombardo Mary-Jane1,Shee Chandan1,Lisewski Andreas M.1,Gonzalez Caleb1,Lin Dongxu1,Nehring Ralf B.1,Saint-Ruf Claude2,Gibson Janet L.1,Frisch Ryan L.1,Lichtarge Olivier13,Hastings P. J.1,Rosenberg Susan M.1345

Affiliation:

1. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030–3411, USA.

2. U1001 INSERM, Université Paris, Descartes, Sorbonne Paris cité, site Necker, 156 rue de Vaugirard, 75730 Paris Cedex 15, France.

3. Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

4. Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA.

5. The Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, TX 77030, USA.

Abstract

Sewing Up DNA Repair All cells have a battery of DNA-repair pathways to help ensure genome maintenance and stability, including stress-induced DNA break repair in Escherichia coli. Similar pathways—which can be mutagenic—are known in yeast and human cells and have the potential to accelerate evolution. Sixteen proteins are known to be required for the pathway in E. coli. Al Mamun et al. (p. 1344 ) analyzed the E. coli pathway to determine the full complement of protein contributions to the pathway. Ninety-three genes were found to be required for stress-induced DNA break repair. One-third of the proteins identified in the network were involved in electron transfer, functioning in oxidative phosphorylation, and acting through the σ s stress response pathway, which thus represents a critical hub in the network.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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