The contribution of recombinationdependent mechanisms to the replication of uv-c damaged dna

MARIA BELEN VALLERGA; MARIA BELEN FEDERICO; SABRINA MANSILLA; JULIANA SPERONI; MARTIN HABIF; VANESA GOTTIFREDI

Ciudad autonoma de Buenos Aires

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

Exposure of cells to genotoxic stimuli causes replication forks stallingat DNA lesions, which might trigger cell death. To preserve viability,cells activate tolerance mechanisms that prevent replication forkcollapse. The best understood tolerance event activated by UVlight is Translesion DNA Synthesis, which aids DNA replicationby recruiting specialized polymerases like pol η to DNA lesions.Another less characterized tolerance event called TemplateSwitching relies on the homology searching capacity of therecombinogenic protein Rad51. In this context, Rad51 facilitatesthe utilization of the novel DNA generated on the opposite strandas alternative template. Other recombinogenic independent functionsof Rad51 have also been reported. In fact, Rad51 protects replicationforks from degradation in a manner that depends on its strandinvasion capacity.Weather any or all of these functions of Rad51 are required afterUVC irradiation is unclear. I will present data of the effect of Rad51depletion 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 ofrecombinogenic and non recombinogenic functions of Rad51 to theresponse of cells to the accumulation of UVC damaged DNA