Department of Life Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva, 84105, Israel; Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva, 84105, Israel.
Graduate Program in Biochemistry and Molecular Biology, University of California, Riverside, CA, 92521, USA; Department of Entomology, University of California, Riverside, CA, 92521, USA.
Insect Biochem Mol Biol. 2019 Mar;106:64-78. doi: 10.1016/j.ibmb.2018.11.009. Epub 2018 Nov 30.
Envenomation of cockroach cerebral ganglia by the parasitoid Jewel wasp, Ampulex compressa, induces specific, long-lasting behavioural changes. We hypothesized that this prolonged action results from venom-induced changes in brain neurochemistry. Here, we address this issue by first identifying molecular targets of the venom, i.e., proteins to which venom components bind and interact with to mediate altered behaviour. Our results show that venom components bind to synaptic proteins and likely interfere with both pre- and postsynaptic processes. Since behavioural changes induced by the sting are long-lasting and reversible, we hypothesized further that long-term effects of the venom must be mediated by up or down regulation of cerebral ganglia proteins. We therefore characterize changes in cerebral ganglia protein abundance of stung cockroaches at different time points after the sting by quantitative mass spectrometry. Our findings indicate that numerous proteins are differentially expressed in cerebral ganglia of stung cockroaches, many of which are involved in signal transduction, such as the Rho GTPase pathway, which is implicated in synaptic plasticity. Altogether, our data suggest that the Jewel wasp commandeers cockroach behaviour through molecular cross-talk between venom components and molecular targets in the cockroach central nervous system, leading to broad-based alteration of synaptic efficacy and behavioural changes that promote successful development of wasp progeny.
美洲大蠊大脑神经节被寄生蜂 Jewel wasp（ Ampulex compressa ）螫刺后会产生特定的、持久的行为变化。我们假设这种长期作用是由毒液引起的大脑神经化学变化所致。在这里，我们通过首先确定毒液的分子靶标来解决这个问题，即毒液成分与之结合并相互作用以介导改变行为的蛋白质。我们的结果表明，毒液成分与突触蛋白结合，并可能干扰突触前和突触后过程。由于毒液引起的行为变化是持久和可逆的，我们进一步假设毒液的长期作用必须通过大脑神经节蛋白的上调或下调来介导。因此，我们通过定量质谱法在螫刺后不同时间点表征被螫刺的蟑螂大脑神经节中的蛋白质丰度变化。我们的发现表明，被螫刺的蟑螂大脑神经节中许多参与信号转导的蛋白质（如参与突触可塑性的 Rho GTPase 途径）表达水平存在差异。总的来说，我们的数据表明，美洲大蠊通过毒液成分与蟑螂中枢神经系统中的分子靶标之间的分子串扰来控制蟑螂的行为，导致突触效能的广泛改变和促进寄生蜂后代成功发育的行为变化。
