Intragenic and extragenic suppression of a mutation in herpes simplex virus 1 UL34 that affects both nuclear envelope targeting and membrane budding.
Intragenic and extragenic suppression of a mutation in herpes simplex virus 1 UL34 that affects both nuclear envelope targeting and membrane budding.
复制标题
单纯疱疹病毒 1 UL34 突变的基因内和基因外抑制，该突变影响核膜靶向和膜出芽。
DOI：
10.1128/jvi.05730-11
复制
发表时间：
2011
影响因子：
5.4
通讯作者：
Kopping,NoraJ
中科院分区：
文献类型：
--
作者：
Roller,RichardJ;Haugo,AlisonC;Kopping,NoraJ
Late in infection herpesviruses move DNA-filled capsids from the nucleus to the cytoplasm by enveloping DNA-containing capsids at the inner nuclear membrane (INM) and deenveloping them at the outer nuclear membrane. This process requires two conserved herpesvirus proteins, pUL31 and pUL34. Interaction between pUL34 and pUL31 is essential for targeting both proteins to the nuclear envelope (NE), and sequences that mediate the targeting interaction have been mapped in both proteins. Here, we show that a mutation in the INM-targeting domain of pUL34 fails to support production of infectious virus or plaque formation. The mutation results in multiple defects, including impaired interaction between pUL34 and pUL31, poor NE targeting of pUL34, and misregulated, capsid-independent budding of the NE. The mutant defects in virus production, plaque formation, and pUL31 interaction can be suppressed by other mutations in the INM-targeting domain of pUL31 and by additional mutations in the pUL34 coding sequence.
