病理相关醛糖和环境醛通过甲酰基介导的机制引起纤毛的破坏。

IF 5.3 2区 生物学 Q2 CELL BIOLOGY Journal of Molecular Cell Biology Pub Date : 2024-07-01 DOI:10.1093/jmcb/mjad079
Te Li, Min Liu, Fan Yu, Song Yang, Weiwen Bu, Kai Liu, Jia Yang, Hua Ni, Mulin Yang, Hanxiao Yin, Renjie Hong, Dengwen Li, Huijie Zhao, Jun Zhou
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引用次数: 0

摘要

碳水化合物代谢紊乱(CMDs),如糖尿病、半乳糖血症和甘露糖病,可引起纤毛病样多器官缺陷。然而,纤毛与CMD并发症的机制联系仍然知之甚少。在这里,我们描述了在病理相关醛糖而不是相应的糖醇处理细胞时显著的纤毛解体。此外,环境醛能够通过其甲酰基的空间位阻效应引发纤毛的分解。机制研究表明,醛刺激细胞外钙通过质膜流入,随后激活钙调素-极光a组蛋白去乙酰化酶6途径,使轴突微管去乙酰化并引发纤毛分解。体内实验进一步表明,Hdac6基因敲除小鼠对醛诱导的气管纤毛和精子鞭毛的脱落具有抗性。这些发现揭示了甲酰基介导的纤毛脱落在CMDs并发症中的作用。
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Pathologically relevant aldoses and environmental aldehydes cause cilium disassembly via formyl group-mediated mechanisms.

Carbohydrate metabolism disorders (CMDs), such as diabetes, galactosemia, and mannosidosis, cause ciliopathy-like multiorgan defects. However, the mechanistic link of cilia to CMD complications is still poorly understood. Herein, we describe significant cilium disassembly upon treatment of cells with pathologically relevant aldoses rather than the corresponding sugar alcohols. Moreover, environmental aldehydes are able to trigger cilium disassembly by the steric hindrance effect of their formyl groups. Mechanistic studies reveal that aldehydes stimulate extracellular calcium influx across the plasma membrane, which subsequently activates the calmodulin-Aurora A-histone deacetylase 6 pathway to deacetylate axonemal microtubules and triggers cilium disassembly. In vivo experiments further show that Hdac6 knockout mice are resistant to aldehyde-induced disassembly of tracheal cilia and sperm flagella. These findings reveal a previously unrecognized role for formyl group-mediated cilium disassembly in the complications of CMDs.

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来源期刊
CiteScore
9.60
自引率
1.80%
发文量
1383
期刊介绍: The Journal of Molecular Cell Biology ( JMCB ) is a full open access, peer-reviewed online journal interested in inter-disciplinary studies at the cross-sections between molecular and cell biology as well as other disciplines of life sciences. The broad scope of JMCB reflects the merging of these life science disciplines such as stem cell research, signaling, genetics, epigenetics, genomics, development, immunology, cancer biology, molecular pathogenesis, neuroscience, and systems biology. The journal will publish primary research papers with findings of unusual significance and broad scientific interest. Review articles, letters and commentary on timely issues are also welcome. JMCB features an outstanding Editorial Board, which will serve as scientific advisors to the journal and provide strategic guidance for the development of the journal. By selecting only the best papers for publication, JMCB will provide a first rate publishing forum for scientists all over the world.
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