Bursicon-α subunit modulates dLGR2 activity in the adult <i>Drosophila melanogaster</i> midgut independently to Bursicon-β

Bursicon is the main regulator of post molting and post eclosion processes during arthropod development. The active Bursicon hormone is a heterodimer of Burs-α and Burs-β. However, adult midguts express Burs-α to regulate the intestinal stem cell niche. Here, we examined the potential expression and function of its heterodimeric partner, Burs-β in the adult midgut. Unexpectedly, our evidence suggests that Burs-β is not significantly expressed in the adult midgut. <i>burs</i>-β mutants displayed the characteristic developmental defects but showed wild type-like adult midguts, thus uncoupling the developmental and adult phenotypes seen in <i>burs</i>-α mutants. Gain of function data and <i>ex vivo</i> experiments using a cAMP biosensor, demonstrated that Burs-α is sufficient to drive stem cell quiescence and to activate dLGR2 in the adult midgut. Our evidence suggests that the post developmental transactivation of dLGR2 in the adult midgut is mediated by Burs-α and that the β subunit of Bursicon is dispensable for these activities.鞣化激素（Bursicon）是节肢动物发育过程中蜕皮后（post molting）与羽化后（post eclosion）过程的主要调控因子。活性鞣化激素为Burs-α与Burs-β构成的异二聚体。然而，成体中肠（adult midgut）可表达Burs-α以调控肠干细胞微环境（intestinal stem cell niche）。本研究探究了其异二聚体伴侣蛋白Burs-β在成体中肠中的潜在表达与功能。出乎意料的是，我们的实验证据表明，Burs-β在成体中肠中无显著表达。*burs-β*突变体表现出典型的发育缺陷，但成体中肠表型与野生型一致，因此将burs-α突变体中观察到的发育表型与成体表型解耦联。功能获得性（gain of function）实验及使用环磷酸腺苷（cAMP）生物传感器的离体（ex vivo）实验证实，仅Burs-α即可驱动成体中肠内的干细胞静息（stem cell quiescence）并激活dLGR2。我们的证据表明，成体中肠内dLGR2的发育后反式激活由Burs-α介导，且鞣化激素的β亚基对于上述功能并非必需。