Exportin-1 is required for the maintenance of the planarian epidermal lineage
Exportin-1 is required for the maintenance of the planarian epidermal lineage
复制标题
Exportin-1 是维持涡虫表皮谱系所必需的
DOI：
10.1016/j.ijbiomac.2019.01.014
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发表时间：
2019
影响因子：
8.2
通讯作者：
Zhang Shoutao
中科院分区：
文献类型：
--
作者：
Tian Qingnan;Zhao Guixia;Sun Yujia;Yuan D;an;Guo Qi;Zhang Yizhe;Liu Jiaqian;Zhang Shoutao
核质转运对于介导从细胞质到细胞核的货物转运的正常细胞功能是必需的。然而，整合干细胞发育的核质转运机制在很大程度上仍然未知。由于其具有大量的干细胞群体，因此，扁形涡虫是研究体内成体干细胞谱系发育的理想系统。在这里，我们集中在exportin-1，这是最保守的核输出受体。目前尚不清楚exportin-1的同源物在干细胞生物学中的作用。针对exportin-1的RNA干扰导致前部和后部再生失败，并导致完整和再生扁形虫的卷曲和溶解表型。在表达过程中，细胞分裂明显减少，表皮细胞标志物（波形蛋白和层粘连蛋白B）的表达从完整的机体中消失。此外，新生细胞标志物piwiA的表达水平降低。相比之下，表皮祖细胞标记物NB 21.11e和AGAT 1的表达水平增加。这些结果表明exportin-1是维持真涡虫表皮谱系所必需的。抑制exportin-1可促进新生细胞向表皮细胞系的过早分化，破坏正常的表皮成熟。
Nucleocytoplasmic transport is essential for normal cellular function that mediates cargo transport from the cytoplasm to the nucleus. However, the mechanisms of nucleocytoplasmic transport that integrate stem cell development remain largely unknown. Since it has a large population of stem cells, the planarian flatworm is an ideal system for the study of adult stem cell lineage development in vivo. Here, we focus onexportin-1, which is the most conserved nuclear export receptor. Homologs ofexportin-1have no currently known role in stem cell biology. RNA interference targetingexportin-1caused a failure in anterior and posterior regeneration, and resulted in curly and lysis phenotypes in both intact and regenerating flatworms. During the course ofexportin-1RNAi phenotype, cell division was significantly decreased, and the expression of the epidermal cell markers (vimentinandlaminB) were lost from the intact body. Additionally, the expression levels of the neoblast marker piwiA decreased. By contrast, the expression levels of the epidermal progenitor markersNB21.11eandAGAT1increased. These results suggest thatexportin-1is required for the maintenance of the epidermal lineage in planarians. Inhibition ofexportin-1could promote the premature differentiation of neoblasts to the epidermal lineages, disrupting the proper epidermal maturation.