HSPD1-facilitated formation of CTPS cytoophidia promotes proliferation in C2C12 cells

IF 3.5 3区 生物学 Q3 CELL BIOLOGY Experimental cell research Pub Date : 2025-03-01 Epub Date: 2025-02-17 DOI:10.1016/j.yexcr.2025.114462
Lili Liu , Wen Chen , Haijing Luo , Weiwei Zhang , Zhenzhu Zhang , Xin Huang , Xuepeng Fu
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Abstract

CTP synthase (CTPS) is a rate-limiting enzyme that controls CTP synthesis and can polymerize to form a filamentous structure called cytoophidia. The presence of cytoophidia affects the enzymatic activity of CTPS. However, whether CTPS can form cytoophidia in C2C12 cells and whether it affects the proliferation of skeletal muscle satellite cells needs to be further studied. In this study, we found that CTPS could form cytoophidia during C2C12 cell proliferation, and that overexpression of CTPS significantly promoted the formation of CTPS cytoophidia and increased the viability and proliferation rate of C2C12 cells. However, the CTPS H355A mutation hindered the formation of CTPS cytoophidia and inhibited the viability and proliferation of C2C12 cells. In addition, we found that the HSPD1 protein could interact with the CTPS protein and interference with Hspd1 gene expression inhibited the formation of CTPS cytoophidia, even with the overexpression of the CTPS gene. Subsequently, it inhibited C2C12 cells proliferation. Thus, these findings reveal the role of CTPS cytoophidia formation in C2C12 cells proliferation.
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hspd1促进CTPS嗜细胞瘤的形成,促进C2C12细胞的增殖
CTP合成酶(CTP synthase, CTPS)是一种限速酶,控制CTP合成,并可聚合形成丝状结构,称为嗜胞丝。嗜细胞质的存在影响CTPS的酶活性。但CTPS是否能在C2C12细胞中形成嗜细胞瘤,是否影响骨骼肌卫星细胞的增殖,还有待进一步研究。在本研究中,我们发现CTPS在C2C12细胞增殖过程中可形成嗜细胞瘤,过表达CTPS可显著促进CTPS嗜细胞瘤的形成,提高C2C12细胞的活力和增殖率。然而,CTPS H355A突变阻碍了CTPS嗜细胞瘤的形成,抑制了C2C12细胞的活力和增殖。此外,我们发现HSPD1蛋白可与CTPS蛋白相互作用,干扰HSPD1基因表达可抑制CTPS嗜细胞瘤的形成,甚至导致CTPS基因过表达。随后抑制C2C12细胞的增殖。因此,这些发现揭示了CTPS嗜细胞瘤的形成在C2C12细胞增殖中的作用。
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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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