Cellular Dynamics of Rad51 and Rad54 in Response to Postreplicative Stress and DNA Damage in HeLa Cells

• Published in: Molecules and cells Vol. 40; no. 2; pp. 143 - 150
• Main Authors: Choi, Eui-Hwan, Yoon, Seobin, Hahn, Yoonsoo, Kim, Keun P
• Format: Journal Article
• Language: English
• Published: United States Korean Society for Molecular and Cellular Biology 01.02.2017; 한국분자세포생물학회
• Subjects: Cell Cycle - genetics; Cell Division - genetics; DNA Damage; DNA Helicases - biosynthesis; DNA Helicases - genetics; DNA-Binding Proteins; G2 Phase - genetics; HeLa Cells; Homologous Recombination; Humans; Nuclear Proteins - biosynthesis; Nuclear Proteins - genetics; Rad51 Recombinase - biosynthesis; Rad51 Recombinase - genetics; Stress, Physiological - genetics; 생물학; Rad51; homologous recombination; Rad54; DNA damage; HeLa cell
• ISSN: 1016-8478; 0219-1032
• DOI: 10.14348/molcells.2017.2275

Homologous recombination (HR) is necessary for maintenance of genomic integrity and prevention of various mutations in tumor suppressor genes and proto-oncogenes. Rad51 and Rad54 are key HR factors that cope with replication stress and DNA breaks in eukaryotes. Rad51 binds to single-stranded DNA (ssDNA) to form the presynaptic filament that promotes a homology search and DNA strand exchange, and Rad54 stimulates the strand-pairing function of Rad51. Here, we studied the molecular dynamics of Rad51 and Rad54 during the cell cycle of HeLa cells. These cells constitutively express Rad51 and Rad54 throughout the entire cell cycle, and the formation of foci immediately increased in response to various types of DNA damage and replication stress, except for caffeine, which suppressed the Rad51-dependent HR pathway. Depletion of Rad51 caused severe defects in response to postreplicative stress. Accordingly, HeLa cells were arrested at the G2-M transition although a small amount of Rad51 was steadily maintained in HeLa cells. Our results suggest that cell cycle progression and proliferation of HeLa cells can be tightly controlled by the abundance of HR proteins, which are essential for the rapid response to postreplicative stress and DNA damage stress.