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一种同时缺失fp25K和p35的家蚕核型多角体病毒突变体的特性分析

Characterization of a Bombyx mori nucleopolyhedrovirus mutant lacking both fp25K and p35.

作者信息

Nakanishi Tadashi, Shimada Toru, Katsuma Susumu

机构信息

Department of Agricultural and Environmental Biology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Yayoi 1-1-1, Bunkyo-ku, Tokyo, 113-8657, Japan.

出版信息

Virus Genes. 2010 Aug;41(1):144-8. doi: 10.1007/s11262-010-0492-5. Epub 2010 May 28.

Abstract

Recent studies have shown that dual mutations in fp25K and p35 of Autographa californica nucleopolyhedrovirus (AcMNPV) result in a typical apoptotic infection on Trichoplusia ni cells, suggesting the involvement of FP25K on NPV-induced apoptosis. To examine the effect of fp25K deletion on Bombyx mori NPV (BmNPV)-induced apoptosis, we generated a BmNPV mutant, fp-p35D, in which both fp25K and p35 genes are deleted from the genome, and compared its phenotype with wild-type (T3), fp25K-deleted (fp-null), and p35-deleted (p35D) BmNPVs. In BmN cells, p35D, but not T3 or fp-null, caused apoptosis with caspase-3 activation. Infection with fp-p35D also resulted in caspase-3 activation, but the level was comparable to that of p35D. Also, we did not observe any apoptotic responses in hemocytes from larvae infected with p35D or fp-p35D. These results indicate that unlike AcMNPV, deletion of fp25K does not affect the pathway of p35D-induced apoptosis of BmN cells and B. mori larvae.

摘要

最近的研究表明,苜蓿银纹夜蛾核型多角体病毒(AcMNPV)的fp25K和p35双突变会导致粉纹夜蛾细胞出现典型的凋亡感染,这表明FP25K参与了NPV诱导的凋亡过程。为了研究fp25K缺失对家蚕核型多角体病毒(BmNPV)诱导凋亡的影响,我们构建了一个BmNPV突变体fp-p35D,其基因组中fp25K和p35基因均被缺失,并将其表型与野生型(T3)、缺失fp25K的(fp-null)和缺失p35的(p35D)BmNPV进行了比较。在BmN细胞中,p35D而非T3或fp-null会通过激活caspase-3导致凋亡。感染fp-p35D也会导致caspase-3激活,但其水平与p35D相当。此外,我们在感染p35D或fp-p35D的幼虫血细胞中未观察到任何凋亡反应。这些结果表明,与AcMNPV不同,fp25K的缺失不会影响p35D诱导BmN细胞和家蚕幼虫凋亡的途径。

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