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Published on: August 20, 2019
Characterization of a Bombyx mori nucleopolyhedrovirus mutant lacking both fp25K and p35
Tadashi Nakanishi1, Toru Shimada, Susumu Katsuma
1Department 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.
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.
Insights
Unlike in AcMNPV, deleting the fp25K gene from BmNPV does not impact apoptosis in silkworm cells or larvae. The p35 gene deletion is the primary driver of apoptosis in Bombyx mori NPV infections.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Autographa californica nucleopolyhedrovirus (AcMNPV) studies suggest FP25K involvement in NPV-induced apoptosis.
- Bombyx mori NPV (BmNPV) is a significant insect pathogen.
Purpose of the Study:
- To investigate the role of the fp25K gene in BmNPV-induced apoptosis.
- To compare the apoptotic effects of BmNPV mutants lacking fp25K, p35, or both genes.
Main Methods:
- Generation of a BmNPV mutant (fp-p35D) lacking both fp25K and p35 genes.
- Phenotypic comparison of fp-p35D with wild-type (T3), fp-null, and p35D BmNPVs in BmN cells and B. mori larvae.
- Assay for caspase-3 activation and observation of apoptotic responses.
Main Results:
- Deletion of p35 (p35D) induced apoptosis with caspase-3 activation in BmN cells.
- The fp-p35D mutant also caused caspase-3 activation, comparable to p35D.
- Neither p35D nor fp-p35D induced apoptosis in hemocytes from infected larvae.
- Deletion of fp25K alone (fp-null) did not cause apoptosis in BmN cells.
Conclusions:
- Unlike AcMNPV, fp25K deletion does not influence BmNPV-induced apoptosis in BmN cells.
- The p35 gene is essential for inhibiting apoptosis in BmNPV infections of BmN cells and B. mori larvae.
- FP25K does not play a significant role in the apoptotic pathway of BmNPV in this context.
