Bradleigh Vinson S, Malva C, Sordetti R, Falabella P, Pennacchio F
Department of Entomology, Texas A & M University, College Station, USA
J Insect Physiol. 1998 Sep;44(9):845-857. doi: 10.1016/s0022-1910(98)00016-x.
Heliothis virescens (F.) last instar larvae parasitized by the endophagous braconid Cardiochiles nigriceps Viereck fail to attain the pupal stage, due to a parasitoid-induced alteration of ecdysteroid biosynthesis and metabolism. Currently available information on host prothoracic gland inactivation in this host-parasitoid system is reported here. Prothoracic glands of H. virescens mature larvae show a depressed biosynthetic activity, without undergoing gross morphological disruption. The ultrastructure of gland cells is characterized by minor parasitoid-induced changes, with the rough endoplasmic reticulum appearing more developed and electrondense than in nonparasitized controls. Eventually, the cells of prothoracic glands of parasitized host last instar larvae die but maintain their structural integrity. The inactivation of pupally committed host prothoracic glands is achieved through the disruption of the PTTH signal transduction pathway. The second messenger cAMP appears to be normally produced in response to PTTH stimulation of glands explanted from parasitized host larvae, however the downstream activation of the cAMP-dependent protein kinase does not appear to occur. In fact, a marked underphosphorylation of regulatory target proteins is observed. This underphosphorylation is associated with a significant reduction in general protein synthesis, which appears to be blocked at the translational level, to a redirection of specific protein synthesis and to a drastic suppression of ecdysteroidogenesis. These parameters appeared to be correlated in a kinetic time-course study, confirming their functional link. C. nigriceps polydnavirus (CnPDV) plays a major role in the inactivation of pupally committed host prothoracic glands, while putative factors occurring in the host haemolymph do not seem to be of particular importance at that developmental stage. Southern blot hybridization indicates the occurrence of PKI(protein kinase inhibitor)-like genes in the C. nigriceps genome, which, in contrast, are undetectable in H. virescens.
被内寄生的茧蜂黑胸茧蜂（Cardiochiles nigriceps Viereck）寄生的烟芽夜蛾（Heliothis virescens (F.)）末龄幼虫无法进入蛹期，这是由于寄生蜂诱导的蜕皮甾体生物合成和代谢改变所致。本文报道了关于该宿主 - 寄生蜂系统中宿主前胸腺失活的现有信息。烟芽夜蛾成熟幼虫的前胸腺显示出生物合成活性降低，且未发生明显的形态破坏。腺细胞的超微结构表现出轻微的寄生蜂诱导变化，粗面内质网比未寄生的对照更发达且电子密度更高。最终，被寄生宿主末龄幼虫的前胸腺细胞死亡，但保持其结构完整性。已进入蛹期的宿主前胸腺的失活是通过破坏促前胸腺激素（PTTH）信号转导途径实现的。第二信使环磷酸腺苷（cAMP）似乎在受到来自被寄生宿主幼虫离体腺体的PTTH刺激时正常产生，然而，依赖cAMP的蛋白激酶的下游激活似乎并未发生。事实上，观察到调节靶蛋白明显的磷酸化不足。这种磷酸化不足与总蛋白合成的显著减少相关，总蛋白合成似乎在翻译水平被阻断，特定蛋白合成发生重定向，蜕皮甾体合成受到剧烈抑制。在动力学时间进程研究中，这些参数似乎相互关联，证实了它们的功能联系。黑胸茧蜂多角体病毒（CnPDV）在已进入蛹期的宿主前胸腺失活中起主要作用，而宿主血淋巴中存在的假定因子在该发育阶段似乎并不特别重要。Southern印迹杂交表明黑胸茧蜂基因组中存在类蛋白激酶抑制剂（PKI）基因，相比之下，在烟芽夜蛾中未检测到这些基因。
