Integrated Ecdysone and O-Linked N-Acetylglucosamine Signaling Coordinates Intestinal Stem Cell Proliferation in Drosophila Midgut.

IF 2.2 3区 生物学 Q3 GENETICS & HEREDITY
Hyun-Jin Na, YiSeul Kim, Jong Min Kim, Mi Jeong Sung, Joung-Sun Park
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Abstract

Steroid hormones and nutrient-sensitive signaling pathways play critical roles in the regulation of stem cell activity, maintenance of tissue homeostasis, and the coordination of metabolic functions. In Drosophila, the steroid hormone ecdysone and the nutrient-responsive post-translational modification O-linked N-acetylglucosamine (O-GlcNAcylation) are emerging as key regulators of intestinal stem cell (ISC) behavior. This study aimed to investigate how the interplay between ecdysone signaling and O-GlcNAcylation controls ISC proliferation and gut homeostasis, particularly in the context of aging. We showed that ecdysone receptor (EcR) expression increases during aging and upon increased O-GlcNAcylation, and that both genetic overexpression of EcR and exogenous 20-hydroxyecdysone treatment promote ISC proliferation and increase O-GlcNAc levels. Conversely, the knockdown of EcR or O-GlcNAc transferase suppressed ISC proliferation and reduced DNA damage accumulation. Our results show that EcR signaling induces DNA damage response and cooperates with O-GlcNAcylation to regulate ISC activity, suggesting a positive feedback loop involving hormones and nutrients. These results highlight the interaction between EcR and O-GlcNAc as a metabolic gatekeeper that balances regenerative activity and genomic integrity in the aging gut. These findings provide a potential mechanistic link for therapeutic strategies for age-related and metabolic diseases involving abnormal stem cell proliferation.

综合蜕皮激素和o -连接n -乙酰氨基葡萄糖信号协调果蝇中肠干细胞增殖。
类固醇激素和营养敏感信号通路在干细胞活性的调节、组织稳态的维持和代谢功能的协调中起着关键作用。在果蝇中,类固醇激素ecdysone和营养反应性翻译后修饰O-linked n -乙酰氨基葡萄糖(o - glcnac酰化)正成为肠干细胞(ISC)行为的关键调节因子。本研究旨在探讨蜕皮激素信号传导和o - glcn酰化之间的相互作用如何控制ISC增殖和肠道稳态,特别是在衰老的背景下。我们发现蜕皮激素受体(EcR)的表达随着年龄的增长和o - glcn酰化的增加而增加,并且EcR的遗传过表达和外源性20-羟基蜕皮激素处理均促进ISC增殖并增加O-GlcNAc水平。相反,敲低EcR或O-GlcNAc转移酶可抑制ISC增殖,减少DNA损伤积累。我们的研究结果表明,EcR信号传导诱导DNA损伤反应,并与o - glcnac酰化协同调节ISC活性,提示一个涉及激素和营养物质的正反馈循环。这些结果强调了EcR和O-GlcNAc之间的相互作用,作为代谢守门人,平衡衰老肠道中的再生活动和基因组完整性。这些发现为涉及异常干细胞增殖的年龄相关和代谢性疾病的治疗策略提供了潜在的机制联系。
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来源期刊
G3: Genes|Genomes|Genetics
G3: Genes|Genomes|Genetics GENETICS & HEREDITY-
CiteScore
5.10
自引率
3.80%
发文量
305
审稿时长
3-8 weeks
期刊介绍: G3: Genes, Genomes, Genetics provides a forum for the publication of high‐quality foundational research, particularly research that generates useful genetic and genomic information such as genome maps, single gene studies, genome‐wide association and QTL studies, as well as genome reports, mutant screens, and advances in methods and technology. The Editorial Board of G3 believes that rapid dissemination of these data is the necessary foundation for analysis that leads to mechanistic insights. G3, published by the Genetics Society of America, meets the critical and growing need of the genetics community for rapid review and publication of important results in all areas of genetics. G3 offers the opportunity to publish the puzzling finding or to present unpublished results that may not have been submitted for review and publication due to a perceived lack of a potential high-impact finding. G3 has earned the DOAJ Seal, which is a mark of certification for open access journals, awarded by DOAJ to journals that achieve a high level of openness, adhere to Best Practice and high publishing standards.
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