Spinal muscular atrophy (SMA) is the most common genetic disease in children. SMA is generally caused by mutations in the gene SMN1. The survival of motor neurons (SMN) complex consists of SMN1, Gemins (2–8), and Strap/Unrip. We previously demonstrated smn1 and gemin5 inhibited tissue regeneration in zebrafish. Here we investigated each individual SMN complex member and identified gemin3 as another regeneration-essential gene. These three genes are likely pan-regenerative, since they affect the regeneration of hair cells, liver, and caudal fin. RNA-Seq analysis reveals that smn1, gemin3, and gemin5 are linked to a common set of genetic pathways, including the tp53 and ErbB pathways. Additional studies indicated all three genes facilitate regeneration by inhibiting the ErbB pathway, thereby allowing cell proliferation in the injured neuromasts. This study provides a new understanding of the SMN complex and a potential etiology for SMA and potentially other rare unidentified genetic diseases with similar symptoms.

脊髓性肌萎缩症（SMA）是儿童中最常见的遗传疾病。SMA通常是由SMN1基因突变引起的。运动神经元（SMN）复合体的存活包括SMN1，Gemins（2-8）和Strap / Unrip。我们以前证明smn1和gemin5抑制斑马鱼的组织再生。在这里，我们调查了每个SMN复杂成员，并将gemin3识别为另一个再生必需基因。这三个基因可能泛再生，因为它们影响毛细胞，肝脏和尾鳍的再生。RNA-Seq分析显示smn1，gemin3和gemin5与一组常见的遗传途径相关，包括tp53和ErbB途径。进一步的研究表明，所有三个基因均通过抑制ErbB途径促进再生，从而使受损的神经瘤细胞增殖。这项研究为SMN复合物提供了新的认识，并为SMA以及潜在的其他罕见的具有类似症状的未确认遗传病提供了病因。