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疯帽匠蛋白介导的Notch信号通路调控成年海马神经干细胞的维持。

Lunatic fringe-mediated Notch signaling regulates adult hippocampal neural stem cell maintenance.

作者信息

Semerci Fatih, Choi William Tin-Shing, Bajic Aleksandar, Thakkar Aarohi, Encinas Juan Manuel, Depreux Frederic, Segil Neil, Groves Andrew K, Maletic-Savatic Mirjana

机构信息

Program in Developmental Biology, Baylor College of Medicine, Houston, United States.

Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, United States.

出版信息

Elife. 2017 Jul 12;6:e24660. doi: 10.7554/eLife.24660.

DOI:10.7554/eLife.24660
PMID:28699891
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5531831/
Abstract

Hippocampal neural stem cells (NSCs) integrate inputs from multiple sources to balance quiescence and activation. Notch signaling plays a key role during this process. Here, we report that Lunatic fringe ( a key modifier of the Notch receptor, is selectively expressed in NSCs. Further, Lfng in NSCs and Notch ligands Delta1 and Jagged1, expressed by their progeny, together influence NSC recruitment, cell cycle duration, and terminal fate. We propose a new model in which Lfng-mediated Notch signaling enables direct communication between a NSC and its descendants, so that progeny can send feedback signals to the 'mother' cell to modify its cell cycle status. Lfng-mediated Notch signaling appears to be a key factor governing NSC quiescence, division, and fate.

摘要

海马神经干细胞(NSCs)整合来自多个来源的输入信号以平衡静止和激活状态。Notch信号通路在此过程中起关键作用。在此,我们报告 Lunatic fringe(Notch受体的关键修饰因子)在神经干细胞中选择性表达。此外,神经干细胞中的Lfng与其子代表达的Notch配体Delta1和Jagged1共同影响神经干细胞的募集、细胞周期持续时间和终末命运。我们提出了一个新模型,其中Lfng介导的Notch信号通路使神经干细胞与其子代之间能够直接通信,从而使子代能够向“母”细胞发送反馈信号以改变其细胞周期状态。Lfng介导的Notch信号通路似乎是控制神经干细胞静止、分裂和命运的关键因素。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/132195bdf3b5/elife-24660-fig1-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/7a50708d4d39/elife-24660-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/f2e6dbae7456/elife-24660-fig2-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/0f99a427f086/elife-24660-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/7ec7c75be991/elife-24660-fig3-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/d773bc5b9fc6/elife-24660-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/9371f326afe0/elife-24660-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/245df7fb4f4d/elife-24660-fig5-figsupp1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/999fe118c7fd/elife-24660-fig6.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/09d0df0d1ed0/elife-24660-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/492d/5531831/60619d377459/elife-24660-resp-fig1.jpg

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