2026-09-18T21:42:56Zhttps://dspace.mit.edu/server/oai/requestoai:dspace.mit.edu:1721.1/375762022-01-13T07:54:15Zcom_1721.1_7582com_1721.1_7581col_1721.1_131022
Terry L. Orr-Weaver.
Park, Eugenia Agnes
Massachusetts Institute of Technology. Dept. of Biology.
Massachusetts Institute of Technology. Department of Biology
2007-05-16T19:02:13Z
2007-05-16T19:02:13Z
2006
2006
http://hdl.handle.net/1721.1/37576
85844594
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2006.
Includes bibliographical references.
In mitotic cell cycles, the genome must be replicated fully in each cell cycle to ensure the normal complement of chromosomes. Failure to replicate chromosomes fully or a failure to limit replication to once-per-cell-cycle may lead to aneuploidy and genomic instability. Variants of the archetypal mitotic cell cycle, utilizing conserved cell cycle machinery, are employed during metazoan development to achieve different aims. Endocycles, in which the cell cycle proceeds without complete mitosis, generate polyploidy and are commonly employed to increase metabolic capacity and cell size. D. melanogaster follicle cell gene amplification, in which bi-directional replication occurs in the absence of detectable gap phases, serves to produce large amounts of eggshell proteins and may also serve to regulate transcription. During D. melanogaster embryogenesis, mitotic cell cycles, endocycles and cell cycle exit occur concurrently. We undertook a screen to identify factors affecting developmentally regulated, variant cell cycles during D. melanogaster embryogenesis. We identified a class of mutants with apparently polyploid cells in normally diploid tissues indicating a failure to maintain mitotic cycles.
(cont.) In this class of mutants, we identified and characterized new mutants in pavarotti and tumbleweed, pav3C53 and tum32a-20. These mutants displayed phenotypic defects consistent with failures in cytokinesis. In particular, tum32a'20 displayed multinucleate cells and abnormal telophase spindles. We also describe the identification, cloning and characterization of the first cyclinE mutant to undergo aberrant gene amplification, cyclinE'16. We observed a novel gene amplification defect, dramatically increased replication fork progression in cyclinE1f36/cyclinEP28 and cyclinE1f36/cyclinEP28 follicle cells implicating CyclinE in the regulation of replication fork speed.
by Eugenia Agnes Park.
Ph.D.
153 leaves
eng
Massachusetts Institute of Technology
M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.
http://dspace.mit.edu/handle/1721.1/7582
Biology.
Developmental regulation of DNA replication in Drosophila melanogaster
Developmental regulation of deoxyribonucleic acid replication in D. melanogaster
Thesis
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<Abstract>In mitotic cell cycles, the genome must be replicated fully in each cell cycle to ensure the normal complement of chromosomes. Failure to replicate chromosomes fully or a failure to limit replication to once-per-cell-cycle may lead to aneuploidy and genomic instability. Variants of the archetypal mitotic cell cycle, utilizing conserved cell cycle machinery, are employed during metazoan development to achieve different aims. Endocycles, in which the cell cycle proceeds without complete mitosis, generate polyploidy and are commonly employed to increase metabolic capacity and cell size. D. melanogaster follicle cell gene amplification, in which bi-directional replication occurs in the absence of detectable gap phases, serves to produce large amounts of eggshell proteins and may also serve to regulate transcription. During D. melanogaster embryogenesis, mitotic cell cycles, endocycles and cell cycle exit occur concurrently. We undertook a screen to identify factors affecting developmentally regulated, variant cell cycles during D. melanogaster embryogenesis. We identified a class of mutants with apparently polyploid cells in normally diploid tissues indicating a failure to maintain mitotic cycles.</Abstract>
<Abstract>(cont.) In this class of mutants, we identified and characterized new mutants in pavarotti and tumbleweed, pav3C53 and tum32a-20. These mutants displayed phenotypic defects consistent with failures in cytokinesis. In particular, tum32a'20 displayed multinucleate cells and abnormal telophase spindles. We also describe the identification, cloning and characterization of the first cyclinE mutant to undergo aberrant gene amplification, cyclinE'16. We observed a novel gene amplification defect, dramatically increased replication fork progression in cyclinE1f36/cyclinEP28 and cyclinE1f36/cyclinEP28 follicle cells implicating CyclinE in the regulation of replication fork speed.</Abstract>
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