Nakanishi Tadashi, Shimada Toru, Katsuma Susumu
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.
Virus Genes. 2010 Aug;41(1):144-8. doi: 10.1007/s11262-010-0492-5. Epub 2010 May 28.
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.
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。