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Shirleen Roeder |
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| Professor of Molecular, Cellular&Developmental Biology and Genetics; Investigator, Howard Hughes Medical Institute |
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* B.S. Dalhousie University, 1973
* Ph.D. University of Toronto, 1978
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| Research Interests: | |
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* Meiotic Chromosome Behavior
* Cell Cycle Checkpoints
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| Honors: | |
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* Presidential Young Investigator Award
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Meiosis is a special type of cell division that produces haploid products from diploid parental cells and thus permits sexual reproduction. During the first
division of meiosis, homologous chromosomes pair with each other, undergo high levels of genetic recombination, and then segregate to opposite poles. We are
isolating and characterizing yeast mutants defective in meiosis in order to investigate the molecular mechanisms of meiotic chromosome behavior.
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| Current Research: | |
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The pairing of homologous chromosomes culminates in the formation of an elaborate proteinaceous structure called the synaptonemal complex. This complex
consists of two lateral elements separated by a central region; each lateral element corresponds to the protein backbone of one pair of condensed sister
chromatids. At least three of the genes identified by yeast meiotic mutants encode structural components of the synaptonemal complex. The Zip1 protein
is a building block of the central region, while Red1 is a component of lateral elements. Zip2 is present at sites of synaptic initiation, where it promotes
Zip1 assembly. Using the zip1, red1 and zip2 mutants as tools, we are exploring the functions of the synaptonemal complex. All three
mutants undergo significant levels of recombination, indicating that synapsis is not necessary for meiotic genetic exchange.
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Our mutant hunts have also identified genes involved in recombination. The Msh4 protein is required for wild-type levels of crossing over and localizes to
discrete spots on meiotic chromosomes. These results suggest that Msh4 is a component of the recombination nodules observed in association with the
synaptonemal complex.
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Meiotic crossovers are nonrandomly distributed such that two crossovers rarely occur close to each other and every pair of chromosomes sustains at least one
genetic exchange to promote its correct segregation at meiosis I. Genetic analysis indicates that crossovers are distributed randomly along and among
chromosomes in the zip1 and msh4 mutants. We propose that Msh4 initiates a signal that inhibits crossing over and that this signal travels
along the synaptonemal complex from one crossover site to nearby potential sites of crossing over.
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Chromosome synapsis is preceded by an homology search that aligns chromosomes at a distance. A circular chromosome does not pair efficiently with its
homolog, suggesting a role for telomeres in homolog pairing. This pairing may depend on the meiosis-specific Tam1 protein, which localizes to telomeres.
The con6 mutant undergoes synapsis between nonhomologous chromosomes, indicating that the Con6 protein also participates in pairing.
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Several meiotic mutants (including zip1 and zip2) arrest in meiotic prophase due to a checkpoint triggered by the accumulation of
intermediates in the recombination and/or synapsis pathways. We are isolating mutants that bypass the zip1 arrest in an attempt to identify
genes whose products function at the pachytene checkpoint.
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Electron micrographs of yeast meiotic chromosomes. Meiotic nuclei from wild type (A) and the zip1 mutant (B) were surface spread and stained with
silver nitrate. Bar = 1 micron. |
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| Representative Publications: | |
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Smith, A. V. and Roeder, G. S. The yeast Red1 protein localizes to the axial cores of meiotic chromosomes. J. Cell Biol. 136:957-967,
1997
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| Contact Information: | |
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