Adult stem cells are crucial for the growth, homeostasis and regeneration of adult tissues. Melanocyte (melanophore) stem cells (MSCs), which give rise to pigment cells in vertebrates, are an attractive model for studying the regulation of adult stem cells. In this issue, two papers provide new information about the involvement of signalling by the receptor tyrosine kinases Kit and ErbB in the establishment of MSCs in zebrafish.
On , Christiane Nüsslein-Volhard and colleagues investigate the embryonic origin of the melanophores that emerge during juvenile development and that contribute to the striking colour patterns of adult zebrafish. The researchers identify a small set of melanophore progenitors (MPs) that are established early in embryonic development and that are associated with the segmentally reiterated dorsal root ganglia in the fish. They use lineage analysis and four-dimensional in vivo imaging to show that the progeny of these embryonic MPs spread segmentally and give rise to the melanophores that create the adult melanophore stripes. Other experiments indicate that the MPs require zebrafish kit ligand a (kitlga, also known as slk) to function as MSCs, and that MP establishment depends on ErbB signalling during early embryonic development. Based on their results, the researchers propose that dorsal root ganglia provide a niche for MSCs and suggest that Kit signalling might attract and maintain MSCs in this niche.
On , Thomas O’Reilly-Pol and Stephen Johnson use clonal analysis to investigate which stages of melanocyte regeneration – establishment of MSCs, recruitment of MSCs to produce committed daughter cells, or the proliferation, differentiation and survival of these daughter cells – are affected by Kit signalling deficits; previous work had shown that a reduction in Kit signalling results in dose-dependent reductions of melanocytes during larval regeneration. The researchers show that the reduction in melanocytes in kita mutants is due to a defect in MSC establishment. By contrast, the other stages of melanocyte regeneration are unaffected. Additional analyses indicate that the MSC establishment defect in kita mutants arises from inappropriate differentiation of the MSC lineage, a finding that confirms and extends the results presented by Nüsslein-Volhard and colleagues.
