The Drosophila spinster (spin) mutant was isolated as a mutant that showed abnormal morphology and function in the nervous system. The spin defect induces neural degeneration similar to human lysosomal storage diseases. Various studies have shown that Spin proteins are localized in lysosomes and participate in the late stages of the autophagic process. Vertebrates have three spinster orthologs, Spns1, Spns2, and Spns3. A defect in Spns1 caused a short lifespan with aberrant lysosomal function in zebrafish. Spns2 was originally isolated as the gene responsible for abnormal heart development and was identified as a sphingosine 1-phosphate transporter in zebrafish. An endothelial cell-specific defect in Spns2 resulted in impaired egress of lymphocytes and the prevention of tumor metastasis in mice. Herein, I reviewed the history of spin/Spns research and discussed the conserved and newly diverged spin/Spns function and possible implications for human diseases.

在果蝇老处女（自旋）突变体被分离为突变体表现出异常形态和功能在神经系统。的自旋缺陷诱导神经变性类似于人溶酶体贮积病。各种研究表明，Spin蛋白位于溶酶体中，并参与自噬过程的后期。脊椎动物有三个老处女同源基因，Spns1，Spns2和Spns3。Spns1的缺陷导致斑马鱼的寿命短，溶酶体功能异常。Spns2最初被分离为负责心脏异常发育的基因，被鉴定为斑马鱼中的鞘氨醇1-磷酸转运蛋白。Spns2中的内皮细胞特异性缺陷可导致淋巴细胞流出受损，并预防小鼠的肿瘤转移。在这里，我回顾了自旋/ Spns研究的历史，并讨论了自旋/ Spns保守和新发的功能以及对人类疾病的可能影响。