Premium
Multiploidy formation in mitotic DNA damage response (616.4)
Author(s) -
Hyun SunYi,
Kim HyoJoo,
Jang YoungJoo
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.616.4
Subject(s) - dna damage , mitosis , g2 m dna damage checkpoint , chek1 , microbiology and biotechnology , genome instability , biology , cell cycle checkpoint , dna replication , cell cycle , cytokinesis , dna re replication , dna repair , control of chromosome duplication , dna , genetics , cell division , apoptosis , cell
The maintenance of genomic stability is significantly important in order to transmit the correct genome information to daughter cell. For defense from DNA damage that induces genomic instability, cells establish a checkpoint pathway which recognize DNA damage and arrest cell cycle. When DNA damage generated in mitotic HeLa cells, mitotic kinases are inactivated by ATM/Chk1/PP2A‐manner, and cells progressed into 4N‐DNA G1 phase. After then, cells are accumulated in 8N‐DNA, suggested that the formation of multiploidy during long‐term response on mitotic DNA damage was induced by cytokinesis failure and re‐replication. Cells with p53‐deletion or ‐inactivation is re‐replicated, whereas cells expressing p53‐wild type arrest before initiation of replication cycle by G1 checkpoint. p53 normal cells are removed by apoptosis at earlier stage of mitotic DNA damage in compare with cells with p53‐deficiency or inactivation of p53. These data suggest that although p53 does not interrupt pre‐RC assembly, p53 might be a key factor to block re‐replication by G1 checkpoint activation in mitotic DNA damaged cells. This research was supported by Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning (NRF‐2013R1A1A3007213).