生物
细胞生物学
神经上皮细胞
视网膜
祖细胞
细胞
斑马鱼
视网膜再生
视网膜
细胞生长
神经干细胞
细胞粘附分子
穆勒胶质细胞
细胞粘附
干细胞
再生(生物学)
遗传学
神经科学
生物化学
基因
作者
Yanan Li,Baijie Xu,Mengmeng Jin,Hui Zhang,Ningxin Ren,Jinhui Hu,Jie He
标识
DOI:10.1083/jcb.202204098
摘要
Correct cell number generation is central to tissue development. However, in vivo roles of coordinated proliferation of individual neural progenitors in regulating cell numbers of developing neural tissues and the underlying molecular mechanism remain mostly elusive. Here, we showed that wild-type (WT) donor retinal progenitor cells (RPCs) generated significantly expanded clones in host retinae with G1-lengthening by p15 (cdkn2a/b) overexpression (p15+) in zebrafish. Further analysis showed that cell adhesion molecule 3 (cadm3) was reduced in p15+ host retinae, and overexpression of either full-length or ectodomains of Cadm3 in p15+ host retinae markedly suppressed the clonal expansion of WT donor RPCs. Notably, WT donor RPCs in retinae with cadm3 disruption recapitulated expanded clones that were found in p15+ retinae. More strikingly, overexpression of Cadm3 without extracellular ig1 domain in RPCs resulted in expanded clones and increased retinal total cell number. Thus, homophilic interaction of Cadm3 provides an intercellular mechanism underlying coordinated cell proliferation to ensure cell number homeostasis of the developing neuroepithelia.
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