Characterization of a putative DNA-repair mechanism in Corynebacterium

• Applicant: Professor Dr. Marc Bramkamp
• Subject Area: Metabolism, Biochemistry and Genetics of Microorganisms
• Term: since 2022
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 498531575

The fast and efficient repair of DNA damage is essential for all cells to resume growth and prevent lethal mutations. Because of the universal importance of DNA repair to all cells, many components, such as RecA/Rad51, are ubiquitously found from bacteria to man. Several different systems have evolved that serve to repair different DNA damages, such as base lesions, strand cross-links, DNA-protein crosslinks or single – and double strand breaks. Double strand breaks (DSB) are, when left unrepaired, always lethal and, hence, a severe problem to any cell. Importantly, DSBs can also appear during DNA replication, when replication forks are stalled. Thus, cells encode efficient repair mechanisms to counteract these cytotoxic lesions. Bacterial cells encode a sophisticated response mechanism to DNA damage termed SOS response. The cellular signal for SOS induction is an unusual high level of single stranded DNA. We have identified a LexA regulated operon, termed DipABCD, in Corynebacterium glutamicum. Dip proteins interact with the polar scaffold protein DivIVA and are upregulated upon DNA stress induced by mitomycin C or introduced DSBs by endonulceases (I-SceI). We will analyze the function of the Dip proteins in C. glutamicum and unravel their subcellular dynamics. C. glutamicum is a particularly interesting model system to study DNA repair, because of its unusual subset of DNA repair systems and the absence of a non-homologous end-joining (NHEJ) repair mechanism.

• DFG Programme: Research Grants