Ganesh Nagaraju
IISc, Bengaluru
Ganesh Nagaraju has been a Professor at the Department of Biochemistry, IISc, since 2007. He received his BSc and MSc from the University of Mysore and his PhD (2003) from the Department of Biochemistry, IISc, Bengaluru. He pursued his postdoctoral studies (2003-2007) in DNA repair, genome stability, and cancer biology at Beth Israel Deaconess Medical Centre and Harvard Medical School, Boston, USA, before joining IISc in 2007. His research is focused on DNA damage responses and cancer biology. He is a recipient of several awards and honours, including the K V Giri Memorial Award for best PhD thesis, B M Birla Science Prize in Biology, the National Bioscience Award for Career Development from DBT, Sir C V Raman Young Scientist Award from Government of Kamataka, Shanti Swamp Bhatnagar Prize in Biological Sciences, Sreenivasaya Memorial Award from SBC(I), and Sir J C Bose Fellowship. He is an elected Fellow ofall three major science academies in India. Elected as Fellow in 2023.
Session 2A - Lectures by Fellows and Associates
Appa Rao Podile, University of Hyderabad, Hyderabad
RTELI helicase regulates homologous recombination during DNA replication
Homologous recombination (HR) plays an essential role in the repair of DNA double-strand breaks (DSBs), replication stress responses, and genome maintenance. However, unregulated HR during replication can impair genome duplication and compromise genome stability. Factors and mechanisms underlying HR regulation during DNA replication are largely unclear. Here, we show that RTEL 1, RAD51, and RAD51 paralogs localize to replicating sites upon recovery from replication stress. The absence of RTELI leads to hyper-recombination during replication and affects genome-wide replication, which can be rescued by co-depleting RAD51 and RAD51 paralogs. Interestingly, co-depletion of fork remodelers such as SMARCAL1/ZRANB3/HLTF/FBHl and expression of HR defective RAD51 mutants rescues replication defect in RTELI deficient cells. The anti-recombinase function of RTELI during replication depends on its interaction with PCNA and helicase activity. Together, their data identify a novel role of RTEL 1 helicase in restricting RAD51-mediated fork reversal and HR activity to facilitate error-free genome duplication.