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Deacetylation of BmAda3 is required for cell apoptosis caused by Bombyx mori nucleopolyhedrovirus infection
Archives of Insect Biochemistry and Physiology ( IF 2.2 ) Pub Date : 2021-08-04 , DOI: 10.1002/arch.21838
Yajie Zhu 1, 2 , Miao Hu 1, 2 , Jonas Ngowo 1, 2 , Xu Gao 1, 2 , Xi Chen 1, 2 , Huihui Yan 1, 2 , Wei Yu 1, 2
Affiliation  

Silkworm is not only an ideal insect model with a biological significance, but it is also crucially important in sericulture and bioreactors. Bombyx mori nucleopolyhedrovirus (BmNPV) is a principal pathogen of silkworm. However, the molecular mechanism underlying BmNPV invasion is still unclear. Based on our previous acetylome research findings of B. mori after BmNPV infection, here, we focused on silkworm alteration/deficiency in activation-3 (BmAda3). The acetylation of K124 and K128 were significantly reduced (0.66-fold) upon the virus challenge. Due to the interaction between Ada3 and P53, acetylation-mimic K124Q/K128Q and deacetylation-mimic K124R/K128R mutants of BmAda3 were constructed to explore the roles exerted by the acetylation modification of BmAda3 on P53. Yeast two-hybrid and IP results revealed that both BmAda3 and its deacetylation mutants (K124R/K128R) interacted with P53. Interestingly, we found that the deacetylation mutants (K124R/K128R) of BmAda3 significantly promoted the stability of P53. Since P53 is a proapoptotic factor, cell apoptosis was detected. We established that the deacetylation of BmAda3 at K124/K128 facilitated cellular apoptosis during BmNPV infection. Finally, viral proliferation was analyzed, and the results indicated that virus generation was reduced by K124/K128 deacetylation. Our report, based on the deacetylation of two lysine sites 124/128 of BmAda3, shows possible regulatory pathways of BmNPV proliferation and provides novel insights into the development of antiviral agents.

中文翻译:

家蚕核多角体病毒感染引起的细胞凋亡需要 BmAda3 的去乙酰化

蚕不仅是一种具有生物学意义的理想昆虫模型,而且在养蚕和生物反应器中也至关重要。家蚕核多角体病毒 (BmNPV) 是家蚕的主要病原体。然而,BmNPV入侵的分子机制尚不清楚。基于我们之前对B. mori乙酰化组的研究结果在 BmNPV 感染后,我们在这里重点研究了家蚕改变/缺乏激活 3 (BmAda3)。在病毒攻击后,K124 和 K128 的乙酰化显着降低(0.66 倍)。由于 Ada3 和 P53 之间的相互作用,构建了 BmAda3 的乙酰化模拟 K124Q/K128Q 和脱乙酰化模拟 K124R/K128R 突变体,以探索 BmAda3 乙酰化修饰对 P53 的作用。酵母双杂交和 IP 结果显示 BmAda3 及其脱乙酰化突变体 (K124R/K128R) 与 P53 相互作用。有趣的是,我们发现 BmAda3 的去乙酰化突变体(K124R/K128R)显着促进了 P53 的稳定性。由于 P53 是促凋亡因子,因此检测到细胞凋亡。我们确定 BmAda3 在 K124/K128 处的去乙酰化促进了 BmNPV 感染期间的细胞凋亡。最后,对病毒增殖进行了分析,结果表明 K124/K128 脱乙酰作用减少了病毒的产生。我们的报告基于 BmAda3 的两个赖氨酸位点 124/128 的脱乙酰化,显示了 BmNPV 增殖的可能调控途径,并为抗病毒药物的开发提供了新的见解。
更新日期:2021-09-20
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