THE CONTRIBUTION OF RECOMBINATION DEPENDENT MECHANISMS TO THE REPLICATION OF UV-C DAMAGED DNA

MARÍA BELÉN VALLERGA; MARÍA BELÉN FEDERICO; SABRINA F. MANSILLA; JULIANA SPERONI; MARTÍN HABIF; VANESA GOTTIFREDI

Buenos Aires, Argentina

Congreso; SAIB-49th Annual Meeting - Argentine Society for Biochemistry and Molecular Biology; 2013

SAIB - Argentine Society for Biochemistry and Molecular Biology

Exposure of cells to genotoxic stimuli causes replication forks stalling at DNA lesions, which might trigger cell death. To preserve viability, cells activate tolerance mechanisms that prevent replication fork collapse. The best understood tolerance event activated by UV light is Translesion DNA Synthesis, which aids DNA replication by recruiting specialized polymerases like pol-eta to DNA lesions. Another less characterized tolerance event called Template Switching relies on the homology searching capacity of the recombinogenic protein Rad51. In this context, Rad51 facilitates the utilization of the novel DNA generated on the opposite strand as alternative template. Other recombinogenic independent functions of Rad51 have also been reported. In fact, Rad51 protects replication forks from degradation in a manner that depends on its strand invasion capacity. Weather any or all of these functions of Rad51 are required after UVC irradiation is unclear. I will present data of the effect of Rad51 depletion on the accumulation of a replication stress marker, 53BP1, and on different DNA replication read-outs after UVC irradiation. I will discuss results in the context of the relative contribution of recombinogenic and non recombinogenic functions of Rad51 to the response of cells to the accumulation of UVC damaged DNA.