Damage-induced reactive oxygen species enable zebrafish tail regeneration by repositioning of Hedgehog expressing cells

First author: Maria Montserrat Garcia Romero; Affiliations: The University of Sheffield (谢菲尔德大学): Sheffield, UK

Corresponding author: Henry Hamilton Roehl

Many aquatic (水生的) vertebrates (脊椎动物) have a remarkable ability to regenerate limbs (肢体) and tails after amputation (切断). Previous studies indicate that reactive oxygen species (ROS) signalling initiates regeneration, but the mechanism by which this takes place is poorly understood. Developmental signalling pathways have been shown to have proregenerative roles in many systems. However, whether these are playing roles that are specific to regeneration, or are simply recapitulating their developmental functions is unclear. Here, we analyse zebrafish (斑马鱼) larval (仔鱼) tail regeneration and find evidence that ROS released upon wounding cause repositioning of notochord cells (脊索细胞) to the damage site. These cells secrete Hedgehog ligands that are required for regeneration. Hedgehog signalling is not required for normal tail development suggesting that it has a regeneration-specific role. Our results provide a model for how ROS initiate tail regeneration, and indicate that developmental signalling pathways can play regenerative functions that are not directly related to their developmental roles.

某些水生的脊椎动物具有能够重生切断的肢体和尾巴的能力。先前的研究显示活性氧物质ROS信号转导起始了再生，然而具体的分子机制还不清楚。发育信号通路被认为在许多系统中在再生前发挥作用。然而，这些信号通路是否特异地在再生过程中发挥作用，亦或是仅仅是再次发挥其在发育期的功能还不确定。本文作者对斑马鱼幼仔的断尾再生进行了研究，发现了ROS能够在受伤位置上发挥作用，将脊索细胞重新定位到受伤位置。这些脊索细胞能够释放Hedgehog配体，这对于再生作用是必需的。Hedgehog信号转导对于正常的尾巴发育是不必要的，这说明这些是在再生过程中特异性发生的。本文的研究结果显示了ROS是如何起始斑马鱼尾巴再生过程的，并且揭示了发育信号通路可能会在再生过程中发挥与其在正常发育过程中不一样的功能。

通讯：Henry H. Roehl（https://www.sheffield.ac.uk/bms/research/roehl）

个人简介：1983-1988年，安提阿学院，生物学学士；1990-1994年，威斯康星大学麦迪逊校区，遗传学硕士；1994-1997年，威斯康星大学麦迪逊校区，遗传学博士；1997-2002年，马克斯普朗克研究所，博士后。

研究方向：以斑马鱼为模式动物研究肌肉骨骼发育与疾病。

doi: https://doi.org/10.1038/s41467-018-06460-2

Journal: Nature Communications

Published date: 01 October, 2018

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