4.7 Article

Involvement of Delta/Notch signaling in zebrafish adult pigment stripe patterning

期刊

DEVELOPMENT
卷 141, 期 2, 页码 318-324

出版社

COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/dev.099804

关键词

Delta/Notch signal; Pigment pattern; Turing mechanism

资金

  1. CREST (Core Research for Evolutional Science and Technology) of the Japan Science and Technology Agency
  2. Takeda Science Foundation
  3. National Institutes of Health [R01 GM062182]
  4. Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan [12024046]
  5. Grants-in-Aid for Scientific Research [25111714, 22127001, 23770247, 22127003] Funding Source: KAKEN

向作者/读者索取更多资源

The skin pigment pattern of zebrafish is a good model system in which to study the mechanism of biological pattern formation. Although it is known that interactions between melanophores and xanthophores play a key role in the formation of adult pigment stripes, molecular mechanisms for these interactions remain largely unknown. Here, we show that Delta/Notch signaling contributes to these interactions. Ablation of xanthophores in yellow stripes induced the death of melanophores in black stripes, suggesting that melanophores require a survival signal from distant xanthophores. We found that deltaC and notch1a were expressed by xanthophores and melanophores, respectively. Moreover, inhibition of Delta/Notch signaling killed melanophores, whereas activation of Delta/Notch signaling ectopically in melanophores rescued the survival of these cells, both in the context of pharmacological inhibition of Delta/Notch signaling and after ablation of xanthophores. Finally, we showed by in vivo imaging of cell membranes that melanophores extend long projections towards xanthophores in the yellow stripes. These data suggest that Delta/Notch signaling is responsible for a survival signal provided by xanthophores to melanophores. As cellular projections can enable long-range interaction between membrane-bound ligands and their receptors, we propose that such projections, combined with direct cell-cell contacts, can substitute for the effect of a diffusible factor that would be expected by the conventional reaction-diffusion (Turing) model.

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