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Notch 依赖性和非依赖性 her 基因网络控制斑马鱼丘脑增殖区的神经干细胞和祖细胞。

A network of Notch-dependent and -independent her genes controls neural stem and progenitor cells in the zebrafish thalamic proliferation zone.

机构信息

Developmental Biology, Institute Biology 1, Faculty of Biology, University of Freiburg, Hauptstrasse 1, 79104 Freiburg, Germany.

Spemann Graduate School of Biology and Medicine SGBM, University of Freiburg, Albertstraße 19A, 79104 Freiburg, Germany.

出版信息

Development. 2023 Apr 1;150(7). doi: 10.1242/dev.201301. Epub 2023 Apr 3.

DOI:10.1242/dev.201301
PMID:37009986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10112928/
Abstract

Neural proliferation zones mediate brain growth and employ Delta/Notch signaling and HES/Her transcription factors to balance neural stem cell (NSC) maintenance with the generation of progenitors and neurons. We investigated Notch-dependency and function of her genes in the thalamic proliferation zone of zebrafish larvae. Nine Notch-dependent genes, her2, her4.1-4.5, her12, her15.1-15.2, and two Notch-independent genes, her6 and her9, are differentially expressed and define distinct NSC and progenitor populations. her6 prominently executes patterning information to maintain NSCs and the zona limitans intrathalamica Shh signaling activity. Surprisingly, simultaneous deletion of nine Notch-dependent her genes does not affect NSCs or progenitor formation, and her4 overexpression only caused reduction of ascl1b progenitors. Combined genetic manipulations of Notch-dependent and -independent her genes suggest that her6 in the thalamic proliferation zone prominently maintains NSCs and inhibits NSC-to-progenitor lineage transitions. The her gene network is characterized by redundant gene functions, with Notch-independent her genes better substituting for loss of Notch-dependent her genes than vice versa. Together, her gene regulatory feedback loops and cross-regulation contribute to the observed robustness of NSC maintenance.

摘要

神经增殖区介导大脑生长，并利用 Delta/Notch 信号和 HES/Her 转录因子来平衡神经干细胞（NSC）的维持与祖细胞和神经元的产生。我们研究了 Notch 依赖性和 her 基因在斑马鱼幼虫丘脑增殖区的功能。有九个 Notch 依赖性基因，即 her2、her4.1-4.5、her12、her15.1-15.2，以及两个 Notch 非依赖性基因，即 her6 和 her9，表达不同，定义了不同的 NSC 和祖细胞群体。her6 显著执行模式信息以维持 NSCs 和丘脑限界内的 Shh 信号活性。令人惊讶的是，同时删除九个 Notch 依赖性 her 基因不会影响 NSCs 或祖细胞的形成，而 her4 的过表达仅导致 ascl1b 祖细胞的减少。Notch 依赖性和非依赖性 her 基因的联合遗传操作表明，her6 在丘脑增殖区显著维持 NSCs 并抑制 NSC 向祖细胞谱系的转变。her 基因调控网络的特点是基因功能冗余，Notch 非依赖性 her 基因更好地替代 Notch 依赖性 her 基因的缺失，而不是相反。总之，her 基因的调控反馈环和交叉调控有助于观察到 NSC 维持的稳健性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/30c4d36297d2/develop-150-201301-g11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/a8e482bd210d/develop-150-201301-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/329d9675b5e4/develop-150-201301-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/56ed67354ba3/develop-150-201301-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/36f526a4b4fe/develop-150-201301-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/d95fe28db371/develop-150-201301-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/257cd80906e4/develop-150-201301-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/3e8cae70aad7/develop-150-201301-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/9502fdeccfbf/develop-150-201301-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/cdcdc243e68a/develop-150-201301-g9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/8b04aed5a389/develop-150-201301-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/30c4d36297d2/develop-150-201301-g11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/a8e482bd210d/develop-150-201301-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/329d9675b5e4/develop-150-201301-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/56ed67354ba3/develop-150-201301-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/36f526a4b4fe/develop-150-201301-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/d95fe28db371/develop-150-201301-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/257cd80906e4/develop-150-201301-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/3e8cae70aad7/develop-150-201301-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/9502fdeccfbf/develop-150-201301-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/cdcdc243e68a/develop-150-201301-g9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/8b04aed5a389/develop-150-201301-g10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f746/10112928/30c4d36297d2/develop-150-201301-g11.jpg

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