UMR CNRS 7267 Écologie et Biologie des Interactions, Université de Poitiers, Poitiers, France.
Department of Geobiology, Georg-August-Universität Göttingen, Göttingen, Germany.
Cell Microbiol. 2021 Nov;23(11):e13381. doi: 10.1111/cmi.13381. Epub 2021 Aug 20.
The endosymbiont Wolbachia feminises male isopods by making them refractory to the insulin-like masculinising hormone, which shunts the autocrine development of the androgenic glands. It was, therefore, proposed that Wolbachia silences the IR receptors, either by preventing their expression or by inactivating them. We describe here the two IR paralogs of Armadillidium vulgare. They displayed a conventional structure and belonged to a family widespread among isopods. Av-IR1 displayed an ubiquist expression, whereas the expression of Av-IR2 was restricted to the gonads. Both were constitutively expressed in males and females and throughout development. However, upon silencing, altered gland physiology and gene expression therein suggested antagonistic roles for Av-IR1 (androinhibiting) and Av-IR2 (androstimulating). They may function in tandem with regulating neurohormones, as a conditional platform that conveys insulin signalling. Wolbachia infection did not alter their expression patterns: leaving the IRs unscathed, the bacteria would suppress the secretion of the neurohormones, thus inducing body-wide IR deactivation and feminisation. Adult males injected with Wolbachia acquired an intersexed physiology. Their phenotypes and gene expressions mirrored the silencing of Av-IR1 only, suggesting that imperfect feminisation stems from a flawed invasion of the androstimulating centre, whereas in fully feminised males invasion would be complete in early juveniles. TAKE AWAY: Two antagonistic Insulin Receptors were characterised in Armadillidium vulgare. The IRs were involved in androstimulating and androinhibiting functions. Wolbachia-induced feminisation did not prevent the expression of the IRs. Imperfectly feminised intersexes phenocopied the silencing of Av-IR1 only. Wolbachia would deactivate the IRs by suppressing neurosecretory co-factors.
共生菌沃尔巴克氏体通过使雄性等足目动物对胰岛素样雄性化激素产生抗性，从而使雄性化激素无法发挥作用，从而阻止了雄性腺的自分泌发育，从而使雄性等足目动物雌性化。因此，有人提出沃尔巴克氏体通过阻止其表达或使其失活来沉默胰岛素受体。我们在这里描述了 Armadillidium vulgare 的两个胰岛素受体（IR）基因。它们具有常规结构，属于在等足目动物中广泛存在的一个家族。Av-IR1 显示出广泛的表达，而 Av-IR2 的表达则局限于性腺。在雄性和雌性以及整个发育过程中，这两种受体都呈组成性表达。然而，沉默后，腺体生理学的改变和其中基因的表达表明，Av-IR1（抗雄性）和 Av-IR2（雄性刺激）可能具有拮抗作用。它们可能与神经激素的调节一起发挥作用，作为传递胰岛素信号的条件平台。沃尔巴克氏体感染并未改变它们的表达模式：不影响 IR，细菌会抑制神经激素的分泌，从而导致全身 IR 失活和雌性化。注射沃尔巴克氏体的成年雄性获得了雌雄同体的生理学特征。它们的表型和基因表达与 Av-IR1 的沉默完全一致，这表明不完全的雌性化源于雄性刺激中心的入侵缺陷，而在完全雌性化的雄性中，入侵将在早期幼体中完全发生。结论：在 Armadillidium vulgare 中，两个拮抗的胰岛素受体被鉴定出来。这些受体参与了雄性刺激和雄性抑制功能。沃尔巴克氏体诱导的雌性化并没有阻止 IR 的表达。不完全雌性化的雌雄同体表型仅与 Av-IR1 的沉默有关。沃尔巴克氏体通过抑制神经分泌共因子来使 IR 失活。
