TRIM67 参与调节嗅球中僧帽细胞的稳态和突触发育。

TRIM67 Implicates in Regulating the Homeostasis and Synaptic Development of Mitral Cells in the Olfactory Bulb.

机构信息

Laboratory of Experimental Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China.

Key Laboratory of Animal Disease and Human Health of Sichuan Province, College of Veterinary Medicine, Chengdu 611130, China.

出版信息

Int J Mol Sci. 2023 Aug 30;24(17):13439. doi: 10.3390/ijms241713439.

DOI:10.3390/ijms241713439

PMID:37686246

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10487898/

Abstract

In recent years, olfactory dysfunction has attracted increasingly more attention as a hallmark symptom of neurodegenerative diseases (ND). Deeply understanding the molecular basis underlying the development of the olfactory bulb (OB) will provide important insights for ND studies and treatments. Now, with a genetic knockout mouse model, we show that TRIM67, a new member of the tripartite motif (TRIM) protein family, plays an important role in regulating the proliferation and development of mitral cells in the OB. TRIM67 is abundantly expressed in the mitral cell layer of the OB. The genetic deletion of TRIM67 in mice leads to excessive proliferation of mitral cells in the OB and defects in its synaptic development, resulting in reduced olfactory function in mice. Finally, we show that TRIM67 may achieve its effect on mitral cells by regulating the Semaphorin 7A/Plexin C1 (Sema7A/PlxnC1) signaling pathway.

摘要

近年来，嗅觉功能障碍作为神经退行性疾病（ND）的标志性症状引起了越来越多的关注。深入了解嗅球（OB）发育的分子基础将为 ND 的研究和治疗提供重要的见解。现在，我们使用基因敲除小鼠模型表明，三肽基重复序列 67（TRIM67），一个三联基序（TRIM）蛋白家族的新成员，在调节 OB 中僧帽细胞的增殖和发育中发挥重要作用。TRIM67 在 OB 的僧帽细胞层中大量表达。在小鼠中 TRIM67 的基因缺失导致 OB 中的僧帽细胞过度增殖和其突触发育缺陷，导致小鼠的嗅觉功能下降。最后，我们表明 TRIM67 可能通过调节 Sema7A/Plexin C1（Sema7A/PlxnC1）信号通路来实现对僧帽细胞的作用。