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类固醇激素诱导的无翅配体调节果蝇雌性肠道大小。

Steroid hormone-induced wingless ligands tune female intestinal size in Drosophila.

作者信息

Zipper Lisa, Corominas-Murtra Bernat, Reiff Tobias

机构信息

Department of Biology, Institute of Genetics, The Faculty of Mathematics and Natural Sciences, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

Department of Biology, University of Graz, Graz, Austria.

出版信息

Nat Commun. 2025 Jan 6;16(1):436. doi: 10.1038/s41467-024-55664-2.

Abstract

Female reproduction comes at great expense to energy metabolism compensated by extensive organ adaptations including intestinal size. Upon mating, endocrine signals orchestrate a 30% net increase of absorptive epithelium. Mating increases production of the steroid hormone Ecdysone released by the Drosophila ovaries that stimulates intestinal stem cell (ISC) divisions. Here, we uncover the transcription factor crooked legs (crol) as an intraepithelial coordinator of Ecdysone-induced ISC mitosis. For the precise investigation of non-autonomous factors on ISC behaviour, we establish Rapport, a spatiotemporally-controlled dual expression and tracing system for the analysis of paracrine genetic manipulation while tracing ISC behaviour. Rapport tracing reveals that Ecdysone-induced Crol controls mitogenic Wnt/Wg-ligand expression from epithelial enterocytes activating ISC mitosis. Paracrine Wg stimulation is counterbalanced by Crol-repression of string/CDC25 and CyclinB autonomously in ISC. Rapport-based ISC tumours confirm paracrine stimulation through the Ecdysone-Crol-Wg axis on mitotic behaviour, whereas the autonomous anti-proliferative role of Crol in ISC is conserved in models of colorectal cancer. Finally, mathematical modelling corroborates increasing enterocyte numbers and Wnt/Wg-degradation to set a stable post-mating intestinal size. Together, our findings provide insights into the complex endocrine growth control mechanisms during mating-induced adaptations and might help untangling pleiotropic hormonal effects observed in gastrointestinal tumorigenesis.

摘要

雌性生殖对能量代谢消耗巨大,需通过包括肠道大小在内的广泛器官适应性变化来补偿。交配后,内分泌信号协调使吸收上皮净增加30%。交配会增加果蝇卵巢释放的类固醇激素蜕皮激素的产生,该激素刺激肠道干细胞(ISC)分裂。在此,我们发现转录因子弯腿(crol)是蜕皮激素诱导的ISC有丝分裂的上皮内协调因子。为了精确研究影响ISC行为的非自主因素,我们建立了Rapport,这是一种时空可控的双表达和追踪系统,用于在追踪ISC行为的同时分析旁分泌基因操作。Rapport追踪显示,蜕皮激素诱导的Crol控制上皮肠细胞产生有丝分裂原性Wnt/Wg配体,从而激活ISC有丝分裂。旁分泌Wg刺激在ISC中被Crol对string/CDC25和细胞周期蛋白B的自主抑制所抵消。基于Rapport的ISC肿瘤证实了通过蜕皮激素-Crol-Wg轴对有丝分裂行为的旁分泌刺激,而Crol在ISC中的自主抗增殖作用在结直肠癌模型中是保守的。最后,数学建模证实肠细胞数量增加和Wnt/Wg降解以设定交配后稳定的肠道大小。总之,我们的研究结果为交配诱导适应性过程中复杂的内分泌生长控制机制提供了见解,并可能有助于理清在胃肠道肿瘤发生中观察到的多效性激素效应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd82/11704138/f0c738179ae4/41467_2024_55664_Fig1_HTML.jpg

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