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A chromosome-coupled ubiquitin-proteasome pathway is required for meiotic surveillance 减数分裂监控需要染色体偶联泛素-蛋白酶体途径
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-05 DOI: 10.1038/s41418-024-01375-6
Ruirui Zhang, Bohan Liu, Yuqi Tian, Mingyu Xin, Qian Li, Xiuhua Huang, Yuanyuan Liu, Li Zhao, Feifei Qi, Ruoxi Wang, Xiaoqian Meng, Jianguo Chen, Jun Zhou, Jinmin Gao

Defects in meiotic prophase can cause meiotic chromosome missegregation and aneuploid gamete formation. Meiotic checkpoints are activated in germ cells with meiotic defects, and cells with unfixed errors are eliminated by apoptosis. How such a surveillance process is regulated remains elusive. Here, we report that a chromosome-coupled ubiquitin-proteasome pathway (UPP) regulates meiotic checkpoint activation and promotes germ cell apoptosis in C. elegans meiosis-defective mutants. We identified an F-box protein, FBXL-2, that functions as a core component within the pathway. This chromosome-coupled UPP regulates meiotic DSB repair kinetics and chromosome dynamic behaviors in synapsis defective mutants. Disrupted UPP impairs the axial recruitment of the HORMA domain protein HIM-3, which is required for efficient germ cell apoptosis in synapsis defective mutants. Our data suggest that an efficient chromosome-coupled UPP functions as a part of the meiotic surveillance system by enhancing the integrity of the meiotic chromosome axis.

减数分裂前期的缺陷可导致减数分裂染色体错误分离和非整倍体配子的形成。在存在减数分裂缺陷的生殖细胞中,减数分裂检查点会被激活,错误未被修复的细胞会被细胞凋亡所淘汰。这种监控过程是如何调控的仍是个谜。在这里,我们报告了染色体组偶联泛素-蛋白酶体途径(UPP)调节减数分裂检查点的激活,并促进秀丽隐杆线虫减数分裂缺陷突变体中生殖细胞的凋亡。我们发现了一种 F-box 蛋白 FBXL-2,它是该通路的核心成分。这种与染色体耦合的 UPP 调节减数分裂 DSB 修复动力学以及突触缺陷突变体的染色体动态行为。中断的UPP会影响HORMA结构域蛋白HIM-3的轴向招募,而HIM-3是突触缺陷突变体中有效生殖细胞凋亡所必需的。我们的数据表明,有效的染色体耦合 UPP 可通过增强减数分裂染色体轴的完整性来发挥减数分裂监控系统的作用。
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引用次数: 0
Correction: Exosomal miR-101-3p and miR-423-5p inhibit medulloblastoma tumorigenesis through targeting FOXP4 and EZH2 更正:外泌体 miR-101-3p 和 miR-423-5p 通过靶向 FOXP4 和 EZH2 抑制髓母细胞瘤肿瘤发生。
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-04 DOI: 10.1038/s41418-024-01345-y
Ping Xue, Saihua Huang, Xiao Han, Caiyan Zhang, Lan Yang, Wenfeng Xiao, Jinrong Fu, Hao Li, Yufeng Zhou
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引用次数: 0
Inhibition of inflammatory osteoclasts accelerates callus remodeling in osteoporotic fractures by enhancing CGRP+TrkA+ signaling 通过增强 CGRP+TrkA+ 信号,抑制炎性破骨细胞可加速骨质疏松性骨折的胼胝体重塑
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-02 DOI: 10.1038/s41418-024-01368-5
Yuexia Shu, Zhenyu Tan, Zhen Pan, Yujie Chen, Jielin Wang, Jieming He, Jia Wang, Yuan Wang

Impaired callus remodeling significantly contributes to the delayed healing of osteoporotic fractures; however, the underlying mechanisms remain unclear. Sensory neuronal signaling plays a crucial role in bone repair. In this study, we aimed to investigate the pathological mechanisms hindering bone remodeling in osteoporotic fractures, particularly focusing on the role of sensory neuronal signaling. We demonstrate that in ovariectomized (OVX) mice, the loss of CGRP+TrkA+ sensory neuronal signaling during callus remodeling correlates with increased Cx3cr1+iOCs expression within the bone callus. Conditional knockout of Cx3cr1+iOCs restored CGRP+TrkA+ sensory neuronal, enabling normal callus remodeling progression. Mechanistically, we further demonstrate that Cx3cr1+iOCs secrete Sema3A in the osteoporotic fracture repair microenvironment, inhibiting CGRP+TrkA+ sensory neurons’ axonal regeneration and suppressing nerve–bone signaling exchange, thus hindering bone remodeling. Lastly, in human samples, we observed an association between the loss of CGRP+TrkA+ sensory neuronal signaling and increased expression of Cx3cr1+iOCs. In conclusion, enhancing CGRP+TrkA+ sensory nerve signaling by inhibiting Cx3cr1+iOCs activity presents a potential strategy for treating delayed healing in osteoporotic fractures.

Inhibition of inflammatory osteoclasts enhances CGRP+TrkA+ signaling and accelerates callus remodeling in osteoporotic fractures.

胼胝体重塑受损是骨质疏松性骨折延迟愈合的重要原因,但其潜在机制仍不清楚。感觉神经元信号在骨修复中起着至关重要的作用。在这项研究中,我们旨在研究阻碍骨质疏松性骨折骨重塑的病理机制,尤其关注感觉神经元信号传导的作用。我们证明,在卵巢切除(OVX)小鼠中,胼胝体重塑过程中 CGRP+TrkA+ 感觉神经元信号的缺失与骨胼胝体中 Cx3cr1+iOCs 表达的增加相关。条件性敲除 Cx3cr1+iOCs 可恢复 CGRP+TrkA+ 感觉神经元,从而使胼胝体重塑过程正常进行。从机理上讲,我们进一步证明了 Cx3cr1+iOCs 在骨质疏松性骨折修复微环境中分泌 Sema3A,抑制 CGRP+TrkA+ 感觉神经元轴突再生,抑制神经-骨信号交换,从而阻碍骨重塑。最后,在人体样本中,我们观察到 CGRP+TrkA+ 感觉神经元信号的缺失与 Cx3cr1+iOCs 表达增加之间存在关联。总之,通过抑制 Cx3cr1+iOCs 的活性来增强 CGRP+TrkA+ 感觉神经信号传递是治疗骨质疏松性骨折延迟愈合的一种潜在策略。
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引用次数: 0
Publisher Correction: Cell death as an architect of adult skin stem cell niches 出版商更正:细胞死亡是成人皮肤干细胞龛的建筑师。
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-09-02 DOI: 10.1038/s41418-024-01362-x
Kim Lecomte, Annagiada Toniolo, Esther Hoste
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引用次数: 0
LUBAC enables tumor-promoting LTβ receptor signaling by activating canonical NF-κB LUBAC 通过激活典型的 NF-κB 来实现促进肿瘤的 LTβ 受体信号转导
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-30 DOI: 10.1038/s41418-024-01355-w
Yu-Guang Chen, Eva Rieser, Amandeep Bhamra, Silvia Surinova, Peter Kreuzaler, Meng-Hsing Ho, Wen-Chiuan Tsai, Nieves Peltzer, Diego de Miguel, Henning Walczak
Lymphotoxin β receptor (LTβR), a member of the TNF receptor superfamily (TNFR-SF), is essential for development and maturation of lymphoid organs. In addition, LTβR activation promotes carcinogenesis by inducing a proinflammatory secretome. Yet, we currently lack a detailed understanding of LTβR signaling. In this study we discovered the linear ubiquitin chain assembly complex (LUBAC) as a previously unrecognized and functionally crucial component of the native LTβR signaling complex (LTβR-SC). Mechanistically, LUBAC-generated linear ubiquitin chains enable recruitment of NEMO, OPTN and A20 to the LTβR-SC, where they act coordinately to regulate the balance between canonical and non-canonical NF-κB pathways. Thus, different from death receptor signaling, where LUBAC prevents inflammation through inhibition of cell death, in LTβR signaling LUBAC is required for inflammatory signaling by enabling canonical and interfering with non-canonical NF-κB activation. This results in a LUBAC-dependent LTβR-driven inflammatory, protumorigenic secretome. Intriguingly, in liver cancer patients with high LTβR expression, high expression of LUBAC correlates with poor prognosis, providing clinical relevance for LUBAC-mediated inflammatory LTβR signaling.
淋巴毒素β受体(LTβR)是 TNF 受体超家族(TNFR-SF)的成员,对淋巴器官的发育和成熟至关重要。此外,LTβR 的活化还能通过诱导促炎分泌组来促进癌变。然而,我们目前还缺乏对 LTβR 信号转导的详细了解。在这项研究中,我们发现了线性泛素链组装复合物(LUBAC),它是以前未曾认识到的原生 LTβR 信号传导复合物(LTβR-SC)的一个重要功能成分。从机理上讲,LUBAC 生成的线性泛素链能将 NEMO、OPTN 和 A20 招募到 LTβR-SC,它们在 LTβR-SC 中协调作用,调节规范和非规范 NF-κB 通路之间的平衡。因此,与死亡受体信号不同的是,LUBAC 通过抑制细胞死亡来防止炎症,而在 LTβR 信号中,LUBAC 是炎症信号所必需的,它可以激活规范 NF-κB 并干扰非规范 NF-κB 的激活。这就形成了依赖于 LUBAC 的 LTβR 驱动的炎性原癌基因分泌组。耐人寻味的是,在LTβR高表达的肝癌患者中,LUBAC的高表达与预后不良相关,这为LUBAC介导的LTβR炎症信号转导提供了临床意义。
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引用次数: 0
Gelsolin alleviates rheumatoid arthritis by negatively regulating NLRP3 inflammasome activation 凝胶苷元通过负向调节 NLRP3 炎症小体的激活缓解类风湿性关节炎
IF 12.4 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-24 DOI: 10.1038/s41418-024-01367-6
Jiyeon Lee, Fumiyuki Sasaki, Eri Koike, Minjeong Cho, Yeongun Lee, So Hee Dho, Jina Lee, Eunji Lee, Eri Toyohara, Mika Sunakawa, Mariko Ishibashi, Huynh Hiep Hung, Saki Nishioka, Ritsuko Komine, Chiaki Okura, Masumi Shimizu, Masahito Ikawa, Akihiko Yoshimura, Rimpei Morita, Lark Kyun Kim

Despite numerous biomarkers being proposed for rheumatoid arthritis (RA), a gap remains in our understanding of their mechanisms of action. In this study, we discovered a novel role for gelsolin (GSN), an actin-binding protein whose levels are notably reduced in the plasma of RA patients. We elucidated that GSN is a key regulator of NLRP3 inflammasome activation in macrophages, providing a plausible explanation for the decreased secretion of GSN in RA patients. We found that GSN interacts with NLRP3 in LPS-primed macrophages, hence modulating the formation of the NLRP3 inflammasome complex. Reducing GSN expression significantly enhanced NLRP3 inflammasome activation. GSN impeded NLRP3 translocation to the mitochondria; it contributed to the maintenance of intracellular calcium equilibrium and mitochondrial stability. This maintenance is crucial for controlling the inflammatory response associated with RA. Furthermore, the exacerbation of arthritic symptoms in GSN-deficient mice indicates the potential of GSN as both a diagnostic biomarker and a therapeutic target. Moreover, not limited to RA models, GSN has demonstrated a protective function in diverse disease models associated with the NLRP3 inflammasome. Myeloid cell-specific GSN-knockout mice exhibited aggravated inflammatory responses in models of MSU-induced peritonitis, folic acid-induced acute tubular necrosis, and LPS-induced sepsis. These findings suggest novel therapeutic approaches that modulate GSN activity, offering promise for more effective management of RA and a broader spectrum of inflammatory conditions.

尽管针对类风湿性关节炎(RA)提出了许多生物标志物,但我们对其作用机制的了解仍然存在差距。在这项研究中,我们发现了凝胶蛋白(GSN)的新作用,凝胶蛋白是一种肌动蛋白结合蛋白,在类风湿性关节炎患者血浆中的含量明显降低。我们阐明了GSN是巨噬细胞中NLRP3炎性体活化的关键调节因子,为RA患者GSN分泌减少提供了合理解释。我们发现,在LPS刺激的巨噬细胞中,GSN与NLRP3相互作用,从而调节NLRP3炎性体复合物的形成。减少GSN的表达会明显增强NLRP3炎性体的激活。GSN 阻碍了 NLRP3 向线粒体的转运;它有助于维持细胞内钙平衡和线粒体的稳定性。这种维持对于控制与 RA 相关的炎症反应至关重要。此外,GSN 缺陷小鼠关节炎症状的加重表明,GSN 具有作为诊断生物标志物和治疗靶点的潜力。此外,GSN不仅限于RA模型,还在与NLRP3炎性体相关的多种疾病模型中显示出保护功能。在MSU诱导的腹膜炎、叶酸诱导的急性肾小管坏死和LPS诱导的败血症模型中,髓系细胞特异性GSN基因敲除小鼠表现出加重的炎症反应。这些发现提出了调节 GSN 活性的新型治疗方法,有望更有效地治疗 RA 和更广泛的炎症。
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引用次数: 0
Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease. 硫代硫酸硫基转移酶的缺乏介导了糖尿病肾病肾小管线粒体脂肪酸氧化的功能障碍。
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-22 DOI: 10.1038/s41418-024-01365-8
Jia Xiu Zhang, Pei Pei Chen, Xue Qi Li, Liang Li, Qin Yi Wu, Gui Hua Wang, Xiong Zhong Ruan, Kun Ling Ma

One of the main characteristics of diabetic kidney disease (DKD) is abnormal renal tubular fatty acid metabolism, especially defective fatty acid oxidation (FAO), accelerating tubular injury and tubulointerstitial fibrosis. Thiosulfate sulfurtransferase (TST), a mitochondrial enzyme essential for sulfur transfer, is reduced in metabolic diseases like diabetes and obesity. However, the potential role of TST in regulating fatty acid metabolic abnormalities in DKD remains unclear. Here, our data revealed decreased TST expression in the renal cortex of DKD patients. TST deficiency exacerbated tubular impairment in both diabetic and renal fibrosis mouse models, while sodium thiosulfate treatment or TST overexpression mitigated renal tubular injury with high-glucose exposure. TST downregulation mediated the decrease in S-sulfhydration of very long-chain specific acyl-CoA dehydrogenase, resulting in mitochondrial FAO dysfunction. This sequence of events exacerbates the progression of tubulointerstitial injury in DKD. Together, our findings demonstrate TST as a regulator of renal tubular injury in DKD.

糖尿病肾病(DKD)的主要特征之一是肾小管脂肪酸代谢异常,尤其是脂肪酸氧化(FAO)缺陷,从而加速肾小管损伤和肾小管间质纤维化。硫代硫酸硫基转移酶(TST)是一种线粒体酶,对硫的转移至关重要,但在糖尿病和肥胖症等代谢性疾病中,TST 的活性会降低。然而,TST 在调节 DKD 脂肪酸代谢异常中的潜在作用仍不清楚。在这里,我们的数据显示,DKD 患者肾皮质中的 TST 表达减少。在糖尿病和肾脏纤维化小鼠模型中,TST缺乏会加重肾小管损伤,而硫代硫酸钠治疗或TST过表达会减轻高葡萄糖暴露下的肾小管损伤。TST 的下调介导了极长链特异性酰基-CoA 脱氢酶 S-硫酸化的减少,导致线粒体 FAO 功能障碍。这一系列事件加剧了 DKD 肾小管间质损伤的进展。我们的研究结果证明,TST 是 DKD 肾小管损伤的调节因子。
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引用次数: 0
The PM20D1-NADA pathway protects against Parkinson’s disease PM20D1-NADA通路可预防帕金森病
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-22 DOI: 10.1038/s41418-024-01356-9
Yunying Yang, Sichun Chen, Li Zhang, Guoxin Zhang, Yan Liu, Yiming Li, Li Zou, Lanxia Meng, Ye Tian, Lijun Dai, Min Xiong, Lina Pan, Jing Xiong, Liam Chen, Hua Hou, Zhui Yu, Zhentao Zhang
Parkinson’s disease (PD) is characterized by the selective loss of dopaminergic neurons in the substantia nigra and the accumulation of α-synuclein (α-Syn) aggregates. However, the molecular mechanisms regulating α-Syn aggregation and neuronal degeneration remain poorly understood. The peptidase M20 domain containing 1 (PM20D1) gene lies within the PARK16 locus genetically linked to PD. Single nucleotide polymorphisms regulating PM20D1 expression are associated with changed risk of PD. Dopamine (DA) metabolism and DA metabolites have been reported to regulate α-Syn pathology. Here we report that PM20D1 catalyzes the conversion of DA to N-arachidonoyl dopamine (NADA), which interacts with α-Syn and inhibits its aggregation. Simultaneously, NADA competes with α-Syn fibrils to regulate TRPV4-mediated calcium influx and downstream phosphatases, thus alleviating α-Syn phosphorylation. The expression of PM20D1 decreases during aging. Overexpression of PM20D1 or the administration of NADA in a mouse model of synucleinopathy alleviated α-Syn pathology, dopaminergic neurodegeneration, and motor impairments. These observations support the protective effect of the PM20D1-NADA pathway against the progression of α-Syn pathology in PD.
帕金森病(PD)的特征是黑质中多巴胺能神经元的选择性丧失和α-突触核蛋白(α-Syn)聚集。然而,人们对调节α-Syn聚集和神经元变性的分子机制仍然知之甚少。含肽酶M20结构域1(PM20D1)基因位于与帕金森病有遗传关联的PARK16位点。调节 PM20D1 表达的单核苷酸多态性与 PD 风险的改变有关。据报道,多巴胺(DA)代谢和DA代谢产物可调节α-Syn病理学。在这里,我们报告了 PM20D1 催化 DA 转化为 N-阿拉伯烯酰多巴胺(NADA),NADA 与 α-Syn 相互作用并抑制其聚集。同时,NADA 与 α-Syn 纤维竞争,调节 TRPV4 介导的钙离子流入和下游磷酸酶,从而缓解 α-Syn 磷酸化。在衰老过程中,PM20D1 的表达量会减少。在突触核蛋白病小鼠模型中过表达 PM20D1 或服用 NADA 可减轻α-Syn 病理变化、多巴胺能神经变性和运动障碍。这些观察结果表明,PM20D1-NADA通路对α-Syn病理学在帕金森病中的发展具有保护作用。
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引用次数: 0
CCKBR+ cancer cells contribute to the intratumor heterogeneity of gastric cancer and confer sensitivity to FOXO inhibition CCKBR+癌细胞导致胃癌的瘤内异质性,并赋予其对 FOXO 抑制剂的敏感性。
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-20 DOI: 10.1038/s41418-024-01360-z
Zhenya Tan, Ke Pan, Minqiong Sun, Xianzhu Pan, Zhi Yang, Zhiling Chang, Xue Yang, Jicheng Zhu, Li Zhan, Yakun Liu, Xiaofei Li, Keqiong Lin, Lin Chen, Hui Mo, Wei Luo, Chen Kan, Lunxi Duan, Hong Zheng
The existence of heterogeneity has plunged cancer treatment into a challenging dilemma. We profiled malignant epithelial cells from 5 gastric adenocarcinoma patients through single-cell sequencing (scRNA-seq) analysis, demonstrating the heterogeneity of gastric adenocarcinoma (GA), and identified the CCKBR+ stem cell-like cancer cells associated poorly differentiated and worse prognosis. We further conducted targeted analysis using single-cell transcriptome libraries, including 40 samples, to confirm these screening results. In addition, we revealed that FOXOs are involved in the progression and development of CCKBR+ gastric adenocarcinoma. Inhibited the expression of FOXOs and disrupting cancer cell stemness reduce the CCKBR+ GA organoid formation and impede tumor progression. Mechanically, CUT&Tag sequencing and Lectin pulldown revealed that FOXOs can activate ST3GAL3/4/5 as well as ST6GALNAC6, promoting elevated sialyation levels in CCKBR+ tumor cells. This FOXO-sialyltransferase axis contributes to the maintenance of homeostasis and the growth of CCKBR+ tumor cells. This insight provides novel perspectives for developing targeted therapeutic strategies aimed at the treating CCKBR associated gastric cancer.
异质性的存在使癌症治疗陷入两难境地。我们通过单细胞测序(scRNA-seq)分析了5例胃腺癌患者的恶性上皮细胞,证明了胃腺癌(GA)的异质性,并确定了CCKBR+干细胞样癌细胞与分化差和预后较差有关。我们进一步利用单细胞转录组文库(包括 40 个样本)进行了靶向分析,以证实这些筛选结果。此外,我们还发现 FOXOs 参与了 CCKBR+ 胃腺癌的进展和发展。抑制 FOXOs 的表达和破坏癌细胞干性可减少 CCKBR+ GA 器官样癌的形成并阻碍肿瘤的进展。从机理上讲,CUT&Tag测序和Lectin pulldown发现,FOXO能激活ST3GAL3/4/5和ST6GALNAC6,促进CCKBR+肿瘤细胞中的苷元化水平升高。这一 FOXO-氨酰基转移酶轴有助于维持 CCKBR+ 肿瘤细胞的平衡和生长。这一观点为开发旨在治疗 CCKBR 相关胃癌的靶向治疗策略提供了新的视角。
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引用次数: 0
Adapting cytoskeleton-mitochondria patterning with myocyte differentiation by promyogenic PRR33. 通过原发性 PRR33 使细胞骨架-微粒体模式化与肌细胞分化相适应
IF 13.7 1区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-15 DOI: 10.1038/s41418-024-01363-w
Xuyang Fu, Feng Zhang, Xiaoxuan Dong, Linbin Pu, Yan Feng, Yang Xu, Feng Gao, Tian Liang, Jianmeng Kang, Hongke Sun, Tingting Hong, Yunxia Liu, Hongmei Zhou, Jun Jiang, Deling Yin, Xinyang Hu, Da-Zhi Wang, Jian Ding, Jinghai Chen

Coordinated cytoskeleton-mitochondria organization during myogenesis is crucial for muscle development and function. Our understanding of the underlying regulatory mechanisms remains inadequate. Here, we identified a novel muscle-enriched protein, PRR33, which is upregulated during myogenesis and acts as a promyogenic factor. Depletion of Prr33 in C2C12 represses myoblast differentiation. Genetic deletion of Prr33 in mice reduces myofiber size and decreases muscle strength. The Prr33 mutant mice also exhibit impaired myogenesis and defects in muscle regeneration in response to injury. Interactome and transcriptome analyses reveal that PRR33 regulates cytoskeleton and mitochondrial function. Remarkably, PRR33 interacts with DESMIN, a key regulator of cytoskeleton-mitochondria organization in muscle cells. Abrogation of PRR33 in myocytes substantially abolishes the interaction of DESMIN filaments with mitochondria, leading to abnormal intracellular accumulation of DESMIN and mitochondrial disorganization/dysfunction in myofibers. Together, our findings demonstrate that PRR33 and DESMIN constitute an important regulatory module coordinating mitochondrial organization with muscle differentiation.

肌肉生成过程中协调的细胞骨架-软骨组织对肌肉的发育和功能至关重要。我们对其潜在调控机制的了解仍然不足。在这里,我们发现了一种新的肌肉富集蛋白--PRR33,它在肌肉生成过程中上调并充当原肌纤维生成因子。在 C2C12 中缺失 Prr33 会抑制成肌细胞分化。小鼠基因缺失 Prr33 会缩小肌纤维尺寸并降低肌肉强度。Prr33 突变体小鼠还表现出肌生成障碍和肌肉损伤再生缺陷。相互作用组和转录组分析表明,PRR33 调节细胞骨架和线粒体功能。值得注意的是,PRR33 与 DESMIN 相互作用,DESMIN 是肌肉细胞中细胞骨架-线粒体组织的关键调节因子。在肌细胞中减弱 PRR33 会大大降低 DESMIN 细丝与线粒体的相互作用,从而导致 DESMIN 在细胞内的异常积聚以及肌纤维中线粒体的紊乱/功能障碍。我们的研究结果表明,PRR33 和 DESMIN 构成了协调线粒体组织和肌肉分化的重要调控模块。
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引用次数: 0
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Cell Death and Differentiation
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