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首页> 外文期刊>Virus Genes >Characterization of a Bombyx mori nucleopolyhedrovirus mutant lacking both fp25K and p35
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Characterization of a Bombyx mori nucleopolyhedrovirus mutant lacking both fp25K and p35

机译:缺乏fp25K和p35的家蚕核多角体病毒突变体的表征

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摘要

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.
机译:最近的研究表明,加利福尼亚州Autographa californica核多角体病毒(AcMNPV)的fp25K和p35的双重突变导致Trichoplusia ni细胞典型的凋亡感染,这表明FP25K参与了NPV诱导的细胞凋亡。为了检查fp25K缺失对家蚕NPV(BmNPV)诱导的凋亡的影响,我们生成了一个BmNPV突变体fp-p35D,其中fp25K和p35基因均从基因组中缺失,并将其表型与野生型( T3),删除了fp25K(fp-null)和删除了p35(p35D)的BmNPV。在BmN细胞中,p35D而不是T3或fp-null导致caspase-3激活引起的细胞凋亡。 fp-p35D感染也导致caspase-3活化,但水平与p35D相当。此外,我们在感染p35D或fp-p35D的幼虫的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诱导的BmN细胞和桑蚕芽孢杆菌幼虫凋亡的途径。

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