Hultman Keith A, Budi Erine H, Teasley Daniel C, Gottlieb Andrew Y, Parichy David M, Johnson Stephen L
Department of Genetics, Washington University School of Medicine, St Louis, MO, USA.
PLoS Genet. 2009 Jul;5(7):e1000544. doi: 10.1371/journal.pgen.1000544. Epub 2009 Jul 3.
Adult stem cells are responsible for maintaining and repairing tissues during the life of an organism. Tissue repair in humans, however, is limited compared to the regenerative capabilities of other vertebrates, such as the zebrafish (Danio rerio). An understanding of stem cell mechanisms, such as how they are established, their self-renewal properties, and their recruitment to produce new cells is therefore important for the application of regenerative medicine. We use larval melanocyte regeneration following treatment with the melanocytotoxic drug MoTP to investigate these mechanisms in Melanocyte Stem Cell (MSC) regulation. In this paper, we show that the receptor tyrosine kinase, erbb3b, is required for establishing the adult MSC responsible for regenerating the larval melanocyte population. Both the erbb3b mutant and wild-type fish treated with the ErbB inhibitor, AG1478, develop normal embryonic melanocytes but fail to regenerate melanocytes after MoTP-induced melanocyte ablation. By administering AG1478 at different time points, we show that ErbB signaling is only required for regeneration prior to MoTP treatment and before 48 hours of development, consistent with a role in establishing MSCs. We then show that overexpression of kitla, the Kit ligand, in transgenic larvae leads to recruitment of MSCs, resulting in overproliferation of melanocytes. Furthermore, kitla overexpression can rescue AG1478-blocked regeneration, suggesting that ErbB signaling is required to promote the progression and specification of the MSC from a pre-MSC state. This study provides evidence that ErbB signaling is required for the establishment of adult MSCs during embryonic development. That this requirement is not shared with the embryonic melanocytes suggests that embryonic melanocytes develop directly, without proceeding through the ErbB-dependent MSC. Moreover, the shared requirement of larval melanocyte regeneration and metamorphic melanocytes that develops at the larval-to-adult transition suggests that these post-embryonic melanocytes develop from the same adult MSC population. Lastly, that kitla overexpression can recruit the MSC to develop excess melanocytes raises the possibility that Kit signaling may be involved in MSC recruitment during regeneration.
成体干细胞负责在生物体的生命过程中维持和修复组织。然而,与其他脊椎动物(如斑马鱼)的再生能力相比,人类的组织修复能力有限。因此,了解干细胞机制,如它们如何建立、自我更新特性以及它们被募集以产生新细胞的过程,对于再生医学的应用非常重要。我们使用黑素细胞毒性药物MoTP处理后的幼虫黑素细胞再生来研究黑素细胞干细胞(MSC)调控中的这些机制。在本文中,我们表明受体酪氨酸激酶erbb3b是建立负责再生幼虫黑素细胞群体的成体MSC所必需的。用ErbB抑制剂AG1478处理的erbb3b突变体和野生型鱼都能发育出正常的胚胎黑素细胞,但在MoTP诱导的黑素细胞消融后无法再生黑素细胞。通过在不同时间点施用AG1478,我们表明ErbB信号仅在MoTP处理之前和发育48小时之前的再生过程中是必需的,这与它在建立MSC中的作用一致。然后我们表明,在转基因幼虫中过表达Kit配体kitla会导致MSC的募集,从而导致黑素细胞过度增殖。此外,kitla过表达可以挽救AG1478阻断的再生过程,这表明ErbB信号是促进MSC从前MSC状态向成熟状态进展和分化所必需的。这项研究提供了证据,表明ErbB信号在胚胎发育过程中对于成体MSC的建立是必需的。胚胎黑素细胞不需要这种信号,这表明胚胎黑素细胞是直接发育的,不经过依赖ErbB的MSC阶段。此外,幼虫黑素细胞再生和幼虫向成体转变过程中发育的变态黑素细胞对ErbB信号有共同需求,这表明这些胚胎后黑素细胞是从同一个成体MSC群体发育而来的。最后,kitla过表达能够募集MSC以产生过量黑素细胞,这增加了Kit信号可能参与再生过程中MSC募集的可能性。