A single-point mutation in HCF causes temperature-sensitive cell-cycle arrest and disrupts VP16 function
A single-point mutation in HCF causes temperature-sensitive cell-cycle arrest and disrupts VP16 function
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DOI：
10.1101/gad.11.6.726
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发表时间：
1997-03-15
影响因子：
10.5
通讯作者：
Nishimoto, T
中科院分区：
文献类型：
--
作者：
Goto, H;Motomura, S;Nishimoto, T
温度敏感的BHK 21仓鼠细胞系tsBN 67停止增殖后，在非允许的温度滞后的一个到几个细胞分裂，和被逮捕的细胞显示类似的血清饥饿的细胞的基因表达模式。温度敏感表型是可逆的，并且是由HCF中的位置134处的单个错义突变-脯氨酸变为丝氨酸-引起的，HCF是一种细胞蛋白，其与病毒蛋白VP 16一起激活单纯疱疹病毒（HSV）立即早期基因的转录。tsBN 67 HCE突变也阻止了VP 16在非允许温度下的转录激活。HCE中的相同点突变破坏VP 16功能和细胞周期的发现表明HCE在细胞周期进展中起作用。除了VP 16依赖性转录之外。
The temperature-sensitive BHK21 hamster cell line tsBN67 ceases to proliferate at the nonpermissive temperature after a lag of one to a few cell divisions, and the arrested cells display a gene expression pattern similar to that of serum-starved cells. The temperature-sensitive phenotype is reversible and results from a single missense mutation-proline to serine at position 134-in HCF, a cellular protein that, together with the viral protein VP16, activates transcription of herpes simplex virus (HSV) immediate-early genes. The tsBN67 HCE mutation also prevents VP16 activation of transcription at the nonpermissive temperature. The finding that the same point mutation in HCE disrupts both VP16 function and the cell cycle suggests that HCE plays a role in cell-cycle progression. in addition to VP16-dependent transcription.