PUBLICATION

Id2a influences neuron and glia formation in the zebrafish retina by modulating retinoblast cell cycle kinetics

Authors
Uribe, R.A., and Gross, J.M.
ID
ZDB-PUB-101018-26
Date
2010
Source
Development (Cambridge, England)   137(22): 3763-3774 (Journal)
Registered Authors
Gross, Jeffrey, Uribe, Rosa
Keywords
none
MeSH Terms
  • Animals
  • Cell Cycle
  • Kinetics
  • Neurogenesis*
  • Neuroglia/cytology
  • Neuroglia/metabolism*
  • Neurons/metabolism*
  • Organ Size
  • Retina/cytology
  • Retina/embryology*
  • Retina/metabolism
  • Zebrafish/embryology*
  • Zebrafish/metabolism
PubMed
20943708 Full text @ Development
Abstract
Inhibitor of differentiation (Id) family helix-loop-helix proteins regulate the proliferation, survival and differentiation of numerous cell types during development; however, their functions during retinal development have not been analyzed. Using loss-of-function and overexpression assays in zebrafish, we demonstrate that Id2a levels modulate retinoblast cell cycle kinetics and thereby influence neuron and glia formation in the retina. Id2a-deficient retinas possess increased numbers of cells occupying S phase, at the expense of mitotic cells, and kinetic analyses demonstrate that Id2a is required for S-phase progression and/or the transition from S to M phase. Id2a-dependent defects in retinoblast proliferation lead to microphthalmia and to an absence of nearly all differentiated inner and outer nuclear layer cell types. Overexpression of id2a has the opposite effect on retinoblast cell cycle kinetics: id2a-overexpressing retinoblasts progress from S to M phase more rapidly and they undergo mitosis more frequently, which results in macrophthalmia. Mosaic analyses reveal that Id2a function in facilitating both cell cycle progression and neuronal differentiation in the retina is non-cell-autonomous, suggesting that Id2a functions upstream of the extrinsic pathways that regulate retinogenesis.
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