跨膜蛋白Syndecan是干细胞存活和维持其核特性所必需的。

IF 4 2区 生物学 Q1 GENETICS & HEREDITY
PLoS Genetics Pub Date : 2025-02-06 eCollection Date: 2025-02-01 DOI:10.1371/journal.pgen.1011586
Buffy L Eldridge-Thomas, Jerome G Bohere, Chantal Roubinet, Alexandre Barthelemy, Tamsin J Samuels, Felipe Karam Teixeira, Golnar Kolahgar
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引用次数: 0

摘要

组织维持是由驻留的干细胞,其活动是由微环境线索调节的基础。利用果蝇作为一个简单的模型来识别干细胞行为和体内存活的调节因子,我们已经发现了保守的跨膜蛋白聚糖Syndecan、核特性和干细胞功能之间的新联系。在果蝇中肠中,肠道干细胞中的Syndecan耗竭导致它们从组织中流失,损害组织更新。在细胞水平上,Syndecan的耗竭改变了细胞和细胞核的形状,并导致核层内陷和DNA损伤。在第二个组织,发育中的果蝇大脑中,实时成像显示神经干细胞中的Syndecan缺失导致细胞分裂时出现的核膜重塑缺陷。我们的发现揭示了Syndecan在维持不同干细胞类型的核特性中的新作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The transmembrane protein Syndecan is required for stem cell survival and maintenance of their nuclear properties.

Tissue maintenance is underpinned by resident stem cells whose activity is modulated by microenvironmental cues. Using Drosophila as a simple model to identify regulators of stem cell behaviour and survival in vivo, we have identified novel connections between the conserved transmembrane proteoglycan Syndecan, nuclear properties and stem cell function. In the Drosophila midgut, Syndecan depletion in intestinal stem cells results in their loss from the tissue, impairing tissue renewal. At the cellular level, Syndecan depletion alters cell and nuclear shape, and causes nuclear lamina invaginations and DNA damage. In a second tissue, the developing Drosophila brain, live imaging revealed that Syndecan depletion in neural stem cells results in nuclear envelope remodelling defects which arise upon cell division. Our findings reveal a new role for Syndecan in the maintenance of nuclear properties in diverse stem cell types.

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来源期刊
PLoS Genetics
PLoS Genetics GENETICS & HEREDITY-
自引率
2.20%
发文量
438
期刊介绍: PLOS Genetics is run by an international Editorial Board, headed by the Editors-in-Chief, Greg Barsh (HudsonAlpha Institute of Biotechnology, and Stanford University School of Medicine) and Greg Copenhaver (The University of North Carolina at Chapel Hill). Articles published in PLOS Genetics are archived in PubMed Central and cited in PubMed.
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