Socs3a在斑马鱼造血中是不可缺少的,也是神经肥大形成所必需的。

IF 3.3 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Mohamed Luban Sobah, Clifford Liongue, Alister C Ward
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引用次数: 0

摘要

背景:细胞因子信号传导抑制因子(SOCS)3是一种参与多种关键细胞因子下游重要负反馈回路的调节蛋白,尤其是白细胞介素-6 (IL-6)家族成员。因此,SOCS3已被证明会影响血液和免疫细胞的发育和功能。斑马鱼体内有SOCS3、Socs3a和Socs3b的重复序列,它们都具有保守的功能域。方法:本研究通过使用CRISPR/Cas9创建全基因组敲除,探索斑马鱼Socs3a的作用,重点关注造血和神经肥大形成。结果:成功产生了斑马鱼Socs3a基因敲除突变体。该突变体的特征表明,正常的造血功能没有受到影响,缺乏Socs3a的中性粒细胞在紧急粒细胞生成过程中对损伤或其产生也没有表现出正常的反应。在Socs3a基因敲除的斑马鱼中,神经肥大的形成受到严重影响。结论:斑马鱼Socs3a突变体造血和骨髓功能正常,但侧线神经肥大的形成受到Socs3a缺失的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Socs3a is Dispensable for Zebrafish Hematopoiesis and is Required for Neuromast Formation.

Background: Suppressor of cytokine signaling (SOCS)3 is a regulatory protein that participates in an important negative feedback loop downstream of several critical cytokines, especially members of the interleukin-6 (IL-6) family. As a result, SOCS3 has been shown to impact the development and function of blood and immune cells. Zebrafish harbor duplicates of SOCS3, Socs3a and Socs3b, both of which possess conserved functional domains.

Methods: This study explored the role of zebrafish Socs3a by creating a whole genome knockout using CRISPR/Cas9, with a focus on hematopoiesis and neuromast formation.

Results: A zebrafish Socs3a knockout mutant was successfully generated. Characterization of this mutant revealed that normal hematopoiesis was not impacted nor was neutrophils lacking Socs3a displayed normal responses to injury or their production during emergency granulopoiesis. Neuromast formation was severely impacted in Socs3a knockout zebrafish.

Conclusions: Zebrafish Socs3a mutants display normal hematopoiesis and myeloid function, but the formation of the lateral line neuromast was affected by the absence of Socs3a.

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