PUBLICATION

Asymmetric inheritance of the apical domain and self-renewal of retinal ganglion cell progenitors depend on Anillin function

Authors
Paolini, A., Duchemin, A.L., Albadri, S., Patzel, E., Bornhorst, D., González Avalos, P., Lemke, S., Machate, A., Brand, M., Sel, S., Di Donato, V., Del Bene, F., Zolessi, F.R., Ramialison, M., Poggi, L.
ID
ZDB-PUB-150207-5
Date
2015
Source
Development (Cambridge, England)   142(5): 832-9 (Journal)
Registered Authors
Albadri, Shahad, Brand, Michael, Del Bene, Filippo, Duchemin, Anne-Laure, Machate, Anja, Paolini, Alessio, Patzel, Eva, Poggi, Lucia, Zolessi, Flavio
Keywords
Anillin, Asymmetric cell division, Ath5 (Atoh7), Neurogenesis, Retina development, Apical domain inheritance
MeSH Terms
  • Contractile Proteins/genetics
  • Contractile Proteins/metabolism*
  • Stem Cells/cytology*
  • Stem Cells/metabolism*
  • Microscopy, Confocal
  • Animals
  • Fluorescent Antibody Technique
  • Zebrafish
  • In Situ Hybridization
  • Retinal Ganglion Cells/cytology*
  • Retinal Ganglion Cells/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
(all 13)
PubMed
25655700 Full text @ Development
Abstract
Divisions that generate one neuronal lineage-committed and one self-renewing cell maintain the balance of proliferation and differentiation for the generation of neuronal diversity. The asymmetric inheritance of apical domains and components of the cell division machinery has been implicated in this process, and might involve interactions with cell fate determinants in regulatory feedback loops of an as yet unknown nature. Here, we report the dynamics of Anillin - an essential F-actin regulator and furrow component - and its contribution to progenitor cell divisions in the developing zebrafish retina. We find that asymmetrically dividing retinal ganglion cell progenitors position the Anillin-rich midbody at the apical domain of the differentiating daughter. anillin hypomorphic conditions disrupt asymmetric apical domain inheritance and affect daughter cell fate. Consequently, the retinal cell type composition is profoundly affected, such that the ganglion cell layer is dramatically expanded. This study provides the first in vivo evidence for the requirement of Anillin during asymmetric neurogenic divisions. It also provides insights into a reciprocal regulation between Anillin and the ganglion cell fate determinant Ath5, suggesting a mechanism whereby the balance of proliferation and differentiation is accomplished during progenitor cell divisions in vivo.
Genes / Markers
Figures
Figure Gallery (7 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
cu2TgTransgenic Insertion
    rw021TgTransgenic Insertion
      th241
        Point Mutation
        tud111TgTransgenic Insertion
          uh4TgTransgenic Insertion
            zf514TgTransgenic Insertion
              1 - 6 of 6
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              Human Disease / Model
              No data available
              Sequence Targeting Reagents
              Target Reagent Reagent Type
              anlnMO1-anlnMRPHLNO
              anlnMO2-anlnMRPHLNO
              1 - 2 of 2
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              Fish
              Antibodies
              Orthology
              No data available
              Engineered Foreign Genes
              Marker Marker Type Name
              EGFPEFGEGFP
              GFPEFGGFP
              mCherryEFGmCherry
              RFPEFGRFP
              1 - 4 of 4
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              Mapping
              No data available