<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-09-19T14:41:29Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/57557" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/57557</identifier><datestamp>2022-01-13T07:54:15Z</datestamp><setSpec>com_1721.1_7582</setSpec><setSpec>com_1721.1_7581</setSpec><setSpec>col_1721.1_131022</setSpec></header><metadata><dim:dim xmlns:dim="http://www.dspace.org/xmlns/dspace/dim" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
   <dim:field mdschema="dc" element="contributor" qualifier="advisor" lang="en_US">Angelika Amon.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Carlile, Thomas M. (Thomas Marshal), Jr</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="other" lang="en_US">Massachusetts Institute of Technology. Dept. of Biology.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="department">Massachusetts Institute of Technology. Department of Biology</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2010-08-26T15:27:18Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2010-08-26T15:27:18Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="copyright" lang="en_US">2010</dim:field>
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   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">654109989</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2010.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">This electronic version was submitted by the student author.  The certified thesis is available in the Institute Archives and Special Collections.</dim:field>
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   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">Meiosis is the process by which haploid gametes are produced from a diploid progenitor cell. Accurate completion of the meiotic divisions requires a variety of modifications to the mitotic chromosome segregation machinery, which allow the reductional meiotic chromosome segregation program to occur. Oscillations in the activity of Cyclin- Dependent Kinases (CDKs) drive virtually every event in the mitotic cell cycle, including events such as cell cycle entry, DNA replication, and chromosome segregation. While much is known about the activity of CDKs, the regulation of CDK activity, and the mechanisms by which CDK activity promotes cell cycle events during vegetative growth in Saccharomyces cerevisiae, relatively little is known about the roles of CDKs during the meiotic divisions. This work examines CDK activity during meiosis, the regulation of CDK activity during meiosis, and mechanisms by which CDKs regulate proper meiotic chromosome segregation. First, a striking diversity in Clb-CDK activity is observed during meiosis, including the identification of Clb1-CDK, and Clb3-CDK as meiosis I and meiosis II specific Clb-CDKs respectively. Second, Clb3 protein is shown to be restricted to meiosis II by translational control mediated by the 5'UTR of the CLB3 message. Finally, premature production of Clb3 results in the premature separation of sister-chromatids during meiosis I.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Thomas M. Carlile.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="degree" lang="en_US">Ph.D.</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="extent" lang="en_US">214 p.</dim:field>
   <dim:field mdschema="dc" element="language" qualifier="iso" lang="en_US">eng</dim:field>
   <dim:field mdschema="dc" element="publisher" lang="en_US">Massachusetts Institute of Technology</dim:field>
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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.</dim:field>
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   <dim:field mdschema="dc" element="subject" lang="en_US">Biology.</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">Cyclin-Dependent Kinase regulation and function during meiosis</dim:field>
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   	&lt;Title>Cyclin-Dependent Kinase regulation and function during meiosis&lt;/Title>
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   	&lt;PublicationDate>2010&lt;/PublicationDate>
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        	&lt;DisplayName>Carlile, Thomas M. (Thomas Marshal), Jr&lt;/DisplayName>
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    &lt;Keyword>Biology.&lt;/Keyword>
   	&lt;Abstract>Meiosis is the process by which haploid gametes are produced from a diploid progenitor cell. Accurate completion of the meiotic divisions requires a variety of modifications to the mitotic chromosome segregation machinery, which allow the reductional meiotic chromosome segregation program to occur. Oscillations in the activity of Cyclin- Dependent Kinases (CDKs) drive virtually every event in the mitotic cell cycle, including events such as cell cycle entry, DNA replication, and chromosome segregation. While much is known about the activity of CDKs, the regulation of CDK activity, and the mechanisms by which CDK activity promotes cell cycle events during vegetative growth in Saccharomyces cerevisiae, relatively little is known about the roles of CDKs during the meiotic divisions. This work examines CDK activity during meiosis, the regulation of CDK activity during meiosis, and mechanisms by which CDKs regulate proper meiotic chromosome segregation. First, a striking diversity in Clb-CDK activity is observed during meiosis, including the identification of Clb1-CDK, and Clb3-CDK as meiosis I and meiosis II specific Clb-CDKs respectively. Second, Clb3 protein is shown to be restricted to meiosis II by translational control mediated by the 5&amp;apos;UTR of the CLB3 message. Finally, premature production of Clb3 results in the premature separation of sister-chromatids during meiosis I.&lt;/Abstract>
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