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Drosophila Embryonic Cell-Cycle Mutants
Nearly all cell division mutants in Drosophila were recovered in late larval/pupal lethal screens, with less than 10 embryonic lethal mutants identified, because larval development occurs without a requirement for cell division. Only cells in the nervous system and the imaginal cells that generate t...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Genetics Society of America
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3789813/ https://www.ncbi.nlm.nih.gov/pubmed/23979936 http://dx.doi.org/10.1534/g3.113.007880 |
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author | Unhavaithaya, Yingdee Park, Eugenia A. Royzman, Irena Orr-Weaver, Terry L. |
author_facet | Unhavaithaya, Yingdee Park, Eugenia A. Royzman, Irena Orr-Weaver, Terry L. |
author_sort | Unhavaithaya, Yingdee |
collection | PubMed |
description | Nearly all cell division mutants in Drosophila were recovered in late larval/pupal lethal screens, with less than 10 embryonic lethal mutants identified, because larval development occurs without a requirement for cell division. Only cells in the nervous system and the imaginal cells that generate the adult body divide during larval stages, with larval tissues growing by increasing ploidy rather than cell number. Thus, most mutants perturbing mitosis or the cell cycle do not manifest a phenotype until the adult body differentiates in late larval and pupal stages. To identify cell-cycle components whose maternal pools are depleted in embryogenesis or that have specific functions in embryogenesis, we screened for mutants defective in cell division during embryogenesis. Five new alleles of Cyclin E were recovered, ranging from a missense mutation that is viable to stop codons causing embryonic lethality. These permitted us to investigate the requirements for Cyclin E function in neuroblast cell fate determination, a role previously shown for a null Cyclin E allele. The mutations causing truncation of the protein affect cell fate of the NB6-4 neuroblast, whereas the weak missense mutation has no effect. We identified mutations in the pavarotti (pav) and tumbleweed (tum) genes needed for cytokinesis by a phenotype of large and multinucleate cells in the embryonic epidermis and nervous system. Other mutations affecting the centromere protein CAL1 and the kinetochore protein Spc105R caused mitotic defects in the nervous system. |
format | Online Article Text |
id | pubmed-3789813 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Genetics Society of America |
record_format | MEDLINE/PubMed |
spelling | pubmed-37898132013-10-17 Drosophila Embryonic Cell-Cycle Mutants Unhavaithaya, Yingdee Park, Eugenia A. Royzman, Irena Orr-Weaver, Terry L. G3 (Bethesda) Mutant Screen Report Nearly all cell division mutants in Drosophila were recovered in late larval/pupal lethal screens, with less than 10 embryonic lethal mutants identified, because larval development occurs without a requirement for cell division. Only cells in the nervous system and the imaginal cells that generate the adult body divide during larval stages, with larval tissues growing by increasing ploidy rather than cell number. Thus, most mutants perturbing mitosis or the cell cycle do not manifest a phenotype until the adult body differentiates in late larval and pupal stages. To identify cell-cycle components whose maternal pools are depleted in embryogenesis or that have specific functions in embryogenesis, we screened for mutants defective in cell division during embryogenesis. Five new alleles of Cyclin E were recovered, ranging from a missense mutation that is viable to stop codons causing embryonic lethality. These permitted us to investigate the requirements for Cyclin E function in neuroblast cell fate determination, a role previously shown for a null Cyclin E allele. The mutations causing truncation of the protein affect cell fate of the NB6-4 neuroblast, whereas the weak missense mutation has no effect. We identified mutations in the pavarotti (pav) and tumbleweed (tum) genes needed for cytokinesis by a phenotype of large and multinucleate cells in the embryonic epidermis and nervous system. Other mutations affecting the centromere protein CAL1 and the kinetochore protein Spc105R caused mitotic defects in the nervous system. Genetics Society of America 2013-10-01 /pmc/articles/PMC3789813/ /pubmed/23979936 http://dx.doi.org/10.1534/g3.113.007880 Text en Copyright © 2013 Unhavaithaya et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Unported License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Mutant Screen Report Unhavaithaya, Yingdee Park, Eugenia A. Royzman, Irena Orr-Weaver, Terry L. Drosophila Embryonic Cell-Cycle Mutants |
title | Drosophila Embryonic Cell-Cycle Mutants |
title_full | Drosophila Embryonic Cell-Cycle Mutants |
title_fullStr | Drosophila Embryonic Cell-Cycle Mutants |
title_full_unstemmed | Drosophila Embryonic Cell-Cycle Mutants |
title_short | Drosophila Embryonic Cell-Cycle Mutants |
title_sort | drosophila embryonic cell-cycle mutants |
topic | Mutant Screen Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3789813/ https://www.ncbi.nlm.nih.gov/pubmed/23979936 http://dx.doi.org/10.1534/g3.113.007880 |
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