Heat-induced G1 arrest is dependent on p53 function but not on RB dephosphorylation.
Normal human cells were heat shocked at 43 degrees C for 2 hr and recovered at 37 degrees C. The levels of p53 and p21 reached a maximum approximately 2 and 6 hr after the heat shock, respectively, and these levels were higher than the control level even at 24 hr. The fraction of S phase cells decreased significantly 8 hr after heat shock, and gradually thereafter. Heat-induced G1 arrest was not found in NCI-H1299 and HeLa cells, which are deficient in p53 function, indicating that p53 function is essential for G1 arrest after heat shock. We found little or no change in phosphorylation of retinoblastoma (RB) protein until 12 hr after heat shock, and a significant change at about 24 hr. No change in phosphorylation of RB at serine-780 and serine-795 occurred within 12 hr after heat shock. These results suggest that heat shock induces G1 arrest mediated by p53, but that G1 arrest within 12 hr after heat shock does not require RB dephosphorylation.
Miyakoda
M
M
School of Pharmaceutical Sciences, Nagasaki University, Nagasaki, 852-8521, Japan.
Nakahata
K
K
Suzuki
K
K
Kodama
S
S
Watanabe
M
M
D002460:Cell Line; D019925:Cyclin A / Q000378:metabolism; D016193:G1 Phase / Q000235:genetics*; D006358:Hot Temperature; D006801:Humans; D010766:Phosphorylation; D016160:Retinoblastoma Protein / Q000378:metabolism*; D016196:S Phase; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D020741:rho GTP-Binding Proteins / Q000378:metabolism
D019925:Cyclin A; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; D020741:rho GTP-Binding Proteins