Non-SMC condensin I complex proteins control chromosome segregation and survival of proliferating cells in the zebrafish neural retina
Autor: | Herwig Baier, Sabine Seipold, Paul Goldsmith, William A. Harris, Florian Priller, Salim Abdelilah-Seyfried |
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Přispěvatelé: | Harris, William [0000-0002-9995-8096], Apollo - University of Cambridge Repository |
Jazyk: | angličtina |
Rok vydání: | 2009 |
Předmět: |
Condensin
Apoptosis Retina Sister chromatid segregation Chromosome segregation Prophase Chromosome Segregation Animals Telophase Mitosis lcsh:QH301-705.5 In Situ Hybridization Zebrafish Cell Proliferation Adenosine Triphosphatases biology Zebrafish Proteins Immunohistochemistry Molecular biology Condensin I complex Cell biology DNA-Binding Proteins lcsh:Biology (General) Cardiovascular and Metabolic Diseases Multiprotein Complexes Premature chromosome condensation biology.protein Tumor Suppressor Protein p53 Research Article Developmental Biology |
Zdroj: | BMC Developmental Biology, Vol 9, Iss 1, p 40 (2009) Seipold, Sabine; Priller, Florian C; Goldsmith, Paul; Harris, William A; Baier, Herwig; & Abdelilah-Seyfried, Salim. (2009). Non-SMC condensin I complex proteins control chromosome segregation and survival of proliferating cells in the zebrafish neural retina. BMC Developmental Biology, 9(1), 40. doi: http://dx.doi.org/10.1186/1471-213X-9-40. Retrieved from: http://www.escholarship.org/uc/item/4kd9w5vp BMC Developmental Biology |
Popis: | Background The condensation of chromosomes and correct sister chromatid segregation during cell division is an essential feature of all proliferative cells. Structural maintenance of chromosomes (SMC) and non-SMC proteins form the condensin I complex and regulate chromosome condensation and segregation during mitosis. However, due to the lack of appropriate mutants, the function of the condensin I complex during vertebrate development has not been described. Results Here, we report the positional cloning and detailed characterization of retinal phenotypes of a zebrafish mutation at the cap-g locus. High resolution live imaging reveals that the progression of mitosis between prometa- to telophase is delayed and that sister chromatid segregation is impaired upon loss of CAP-G. CAP-G associates with chromosomes between prometa- and telophase of the cell cycle. Loss of the interaction partners CAP-H and CAP-D2 causes cytoplasmic mislocalization of CAP-G throughout mitosis. DNA content analysis reveals increased genomic imbalances upon loss of non-SMC condensin I subunits. Within the retina, loss of condensin I function causes increased rates of apoptosis among cells within the proliferative ciliary marginal zone (CMZ) whereas postmitotic retinal cells are viable. Inhibition of p53-mediated apoptosis partially rescues cell numbers in cap-g mutant retinae and allows normal layering of retinal cell types without alleviating their aberrant nuclear sizes. Conclusion Our findings indicate that the condensin I complex is particularly important within rapidly amplifying progenitor cell populations to ensure faithful chromosome segregation. In contrast, differentiation of postmitotic retinal cells is not impaired upon polyploidization. |
Databáze: | OpenAIRE |
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