Teratocyte-secreting proteins of an endoparasitoid wasp, Cotesia plutellae, prevent host metamorphosis by altering endocrine signals.

An endoparasitoid wasp, Cotesia plutellae, parasitizes young larvae of the diamondback moth, Plutella xylostella, with its parasitic factors of polydnavirus, venom, ovarian proteins, and teratocytes (TCs). TCs are originated from embryonic serosal membrane at hatch of C. plutellae egg. Injection of in vitro cultured TCs significantly prolonged a larval period of nonparasitized P. xylostella and impaired a larva-to-pupa metamorphosis. This developmental alteration was also induced by injection of TC-cultured medium (TCM). However, heat-treated TCM significantly lost the inhibitory activity against larval development of P. xylostella. Larvae treated with TC or TCM appeared to undergo abnormal endocrine conditions. Juvenile hormone esterase activity was significantly suppressed at early last instar by injection of TC or TCM. In addition, expression of ecdysone receptor at final instar was lost, but that of insulin receptor was maintained until the end of the larval period in TC or TCM treatment. A proteomic analysis of TCM predicted several teratocyte-secreting proteins (TSPs). The inhibitory effect of host development by TCs was significantly enhanced by an addition of another parasitic factor, C. plutellae bracovirus. These results suggest that C. plutellae TC plays a crucial role in alteration of host development by secreting TSPs.