CTPS cytoophidia in Drosophila: distribution, regulation, and physiological roles

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Qingyi Wang , Ji-Long Liu , Jingnan Liu
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引用次数: 0

Abstract

Intracellular compartmentalization plays a critical role in maintaining cellular homeostasis and regulating metabolic processes. A growing body of evidence suggests that various metabolic enzymes, including CTP synthase (CTPS), can dynamically assemble into membraneless filamentous structures. The formation of these membraneless organelles is precisely regulated by the cellular metabolic state. CTPS, a rate-limiting enzyme in the de novo biosynthesis of CTP, has been shown to assemble into filamentous structures known as cytoophidium. First identified in 2010 by three independent research groups, cytoophidia are evolutionarily conserved across diverse organisms, including bacteria, archaea, yeast, mammals, and plants, suggesting a fundamental biological function. Given the well-established advantages of Drosophila melanogaster as a genetic model, this organism provides a powerful system for investigating the physiological roles of cytoophidia. This review synthesizes current findings on CTPS cytoophidia in Drosophila, with a particular focus on their spatiotemporal distribution in tissues and their regulatory roles in three key biological processes: intestinal homeostasis, lipid metabolism, and reproductive physiology. Furthermore, we discuss the challenges and future directions in cytoophidia research, offering insights into their broader implications in cellular metabolism and physiology.
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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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