Feline calicivirus p32, p39 and p30 proteins localize to the endoplasmic reticulum to initiate replication complex formation.
Feline calicivirus p32, p39 and p30 proteins localize to the endoplasmic reticulum to initiate replication complex formation.
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DOI：
10.1099/vir.0.016279-0
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发表时间：
2010-03
期刊：
影响因子：
--
通讯作者：
Goodfellow IG
中科院分区：
文献类型：
--
作者：
Bailey D;Kaiser WJ;Hollinshead M;Moffat K;Chaudhry Y;Wileman T;Sosnovtsev SV;Goodfellow IG
与其他正链RNA病毒一样，猫杯状病毒（FCV）的复制导致细胞内膜重排并产生许多膜结合囊泡结构，病毒基因组复制被认为发生在这些结构上。在这项研究中，生物信息学方法已经确定了三个FCV非结构蛋白，即p32，p39和p30，作为潜在的跨膜蛋白。这些蛋白能够将增强的青色荧光蛋白靶向膜组分，在那里它们表现为整合的膜蛋白。这些蛋白质在细胞中表达的免疫荧光显微镜显示共定位与内质网（ER）标记。对共表达FCV p39或p30与含有KDEL ER保留基序的辣根过氧化物酶蛋白的细胞的进一步电子显微镜分析表明ER的总体形态学变化。在自然感染的Crandel-Rees猫肾细胞中观察到类似的重组模式，特别是p30产生的重组模式。总之，数据表明FCV的p32、p39和p30蛋白定位于ER并导致ER膜的重组。这表明它们可能在FCV复制复合物的产生中起作用，并且内质网可能代表FCV感染期间诱导的膜囊泡的潜在来源。
In common with other positive-strand RNA viruses, replication of feline calicivirus (FCV) results in rearrangement of intracellular membranes and production of numerous membrane-bound vesicular structures on which viral genome replication is thought to occur. In this study, bioinformatics approaches have identified three of the FCV non-structural proteins, namely p32, p39 and p30, as potential transmembrane proteins. These proteins were able to target enhanced cyan fluorescent protein to membrane fractions where they behaved as integral membrane proteins. Immunofluorescence microscopy of these proteins expressed in cells showed co-localization with endoplasmic reticulum (ER) markers. Further electron microscopy analysis of cells co-expressing FCV p39 or p30 with a horseradish peroxidase protein containing the KDEL ER retention motif demonstrated gross morphological changes to the ER. Similar reorganization patterns, especially for those produced by p30, were observed in naturally infected Crandel–Rees feline kidney cells. Together, the data demonstrate that the p32, p39 and p30 proteins of FCV locate to the ER and lead to reorganization of ER membranes. This suggests that they may play a role in the generation of FCV replication complexes and that the endoplasmic reticulum may represent the potential source of the membrane vesicles induced during FCV infection.
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DOI：
10.1083/jcb.93.1.97
发表时间：
1982-04
期刊：
The Journal of cell biology
影响因子：
--
作者：
Fujiki Y;Hubbard AL;Fowler S;Lazarow PB
通讯作者：
Lazarow PB
DOI：
10.1006/bbrc.1995.1010
发表时间：
1995-01-05
影响因子：
3.1
作者：
ALDABE, R;CARRASCO, L
通讯作者：
CARRASCO, L
影响因子：
64.5
作者：
HEBERT, DN;FOELLMER, B;HELENIUS, A
通讯作者：
HELENIUS, A
影响因子：
3.7
作者：
BIENZ, K;EGGER, D;BOSSART, W
通讯作者：
BOSSART, W
影响因子：
5.4
作者：
Doedens, JR;Giddings, TH;Kirkegaard, K
通讯作者：
Kirkegaard, K