TLK1 Phosphorylates RAD54 To Promote Homology Driven DSB Repair
Abstract
Environmental agents like Ionizing radiation (I.R) can cause severe damage to DNA often causing double‐strand break (DSB). If unrepaired, DSB elicits chromosomal rearrangements, tumorigenesis, or apoptosis. The main mechanism to maintain the fidelity of the genetic information after DSBs is homologous recombination repair (HRR). The regulation of this process is unclear. Tousled‐like kinase 1 (TLK1), a Ser/Thr kinase that regulates DNA damage checkpoint and DSB repair has been found to interact with RAD54, a central DNA translocase enzyme in HRR. Our work aims to study how TLK1 regulates RAD54 activities during HRR? We hypothesize that phosphorylation of RAD54 at both NTD and CTD by TLK1 promotes HRR through RAD51‐nucleofilament interaction or during Branch Migration through RAD54 translocase activity.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- May 01, 2022
- Source ID
- 10.1096/fasebj.2022.36.s1.r2792
Entities
People
- Arrigo Debenedetti
- Claudia Wiese
- Ishita Ghosh
- Jing Chen
- Patrick Sung
- Youngho Kwon
Organizations
- Colorado State University
- LSU Health Sciences Center New Orleans
- United States Department of Defense
- University of Kentucky
- University of Texas at Austin