Molecular mechanisms for apoptosis induction and suppression n insect cells infected with nucleopolyhedroviruses

细胞凋亡是杆状病毒感染鳞翅目昆虫细胞的主要防御机制。在本研究中，我们研究了昆虫细胞感染核多角体病毒（NPVs）后诱导和抑制细胞凋亡的分子机制。我们从几种NPV和昆虫细胞中克隆了一些可能在凋亡途径中起作用的细胞和病毒因子的cDNA。这些包括细胞因子Dronc，Caspase-1，IAP，P53，Reaper和Sirt 2，以及病毒因子Apsup和IAP。通过这些因子在瞬时表达实验中的功能分析，我们提供了几个重要的见解，细胞凋亡的诱导和抑制在NPV感染的昆虫细胞的调节机制。我们还证明了IAP 1抑制Dronc活化并促进活化的Dronc的降解以防止非凋亡昆虫细胞中的凋亡诱导。

Apoptosis serves as the major anti-viral defense mechanism in baculovirus-infected lepidopteran insect cells. In the present study, we examined molecular mechanisms underlying induction and inhibition of apoptosis that occur in insect cells upon infection with nucleopolyhedroviruses (NPVs). We cloned a number of cDNAs of cellular and viral factors, which possibly function in the apoptotic pathways, from several NPVs and insect cells. These include cellular factors Dronc, Caspase-1s, IAPs, P53, Reaper and Sirt2, and viral factors Apsup and IAPs. Through functional analysis of these factors in transient expression experiments, we provide several important insights into regulation mechanisms of apoptosis induction and inhibition in NPV-infected insect cells. We also demonstrated that IAP1 inhibits Dronc activation and promotes degradation of activated Dronc to prevent apoptosis induction in non-apoptotic insect cells.