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Arl4aa 在斑马鱼造血起始过程中的功能是通过维持造血内皮细胞中高尔基体复合体的完整性来实现的。

Function of Arl4aa in the Initiation of Hematopoiesis in Zebrafish by Maintaining Golgi Complex Integrity in Hemogenic Endothelium.

机构信息

Division of Haematology, Department of Medicine, The University of Hong Kong, Hong Kong, China; Forward Pharmaceuticals Co., Ltd, Shen Zhen, China.

Division of Haematology, Department of Medicine, The University of Hong Kong, Hong Kong, China.

出版信息

Stem Cell Reports. 2020 Apr 14;14(4):575-589. doi: 10.1016/j.stemcr.2020.02.012. Epub 2020 Mar 26.

DOI:10.1016/j.stemcr.2020.02.012
PMID:32220330
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7160373/
Abstract

ADP-ribosylation factor-like 4aa (Arl4aa) is a member of the ADP-ribosylation factor family. It is expressed in hematopoietic tissue during embryonic development, but its function was unknown. Zebrafish arl4aa is preferentially expressed in the ventral wall of the dorsal aorta (VDA) at 24 and 36 hpf and in caudal hematopoietic tissue at 48 hpf. Morpholino knockdown and transcription activator-like effector nuclease (TALEN) knockout of arl4aa significantly reduced expression of genes associated with definitive hematopoietic stem cells (HSCs). Golgi complex integrity in VDA was disrupted as shown by transmission electron microscopy and immunostaining of Golgi membrane Giantin. Mechanistically, arl4aa knockdown reduced Notch signaling in the VDA and its target gene expression. Protein expression of NICD was also reduced. Effects of arl4aa knockdown on definitive hematopoiesis could be restored by NICD expression. This study identified arl4aa as a factor regulating initiation of definitive HSCs by maintaining the integrity of Golgi complex and, secondarily, maturation of the Notch receptor.

摘要

ADP-核糖基化因子样蛋白 4aa（Arl4aa）是 ADP-核糖基化因子家族的一员。它在胚胎发育过程中的造血组织中表达，但功能未知。斑马鱼 arl4aa 在 24 和 36 hpf 时优先在背主动脉（VDA）的腹侧壁表达，在 48 hpf 时在尾造血组织中表达。Arl4aa 的 morpholino 敲低和转录激活因子样效应物核酸酶（TALEN）敲除显著降低了与确定性造血干细胞（HSCs）相关的基因的表达。电镜和高尔基膜 Giantin 免疫染色显示，VDA 中的高尔基复合体完整性被破坏。在机制上，arl4aa 敲低降低了 VDA 中的 Notch 信号及其靶基因的表达。NICD 的蛋白表达也减少了。通过表达 NICD，可恢复 arl4aa 敲低对确定性造血的影响。这项研究确定 arl4aa 是通过维持高尔基复合体的完整性来调节确定性 HSCs 起始的因素，其次是 Notch 受体的成熟。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/4917196a07d6/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/b516f3e49814/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/64cd47430335/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/5a7163bae56e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/27f15dbb39b0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/a3c4d16e63f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/da0fcf8346e2/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/4917196a07d6/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/b516f3e49814/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/64cd47430335/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/5a7163bae56e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/27f15dbb39b0/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/a3c4d16e63f8/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/da0fcf8346e2/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60ef/7160373/4917196a07d6/gr7.jpg

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