<?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>2026-09-19T10:32:07Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/81031" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/81031</identifier><datestamp>2022-01-13T07:53:55Z</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">Attner, Michelle Andrea</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="other" lang="en_US">Massachusetts Institute of Technology. Department 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">2013-09-24T19:38:11Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2013-09-24T19:38:11Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="issued" lang="en_US">2013</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="uri">http://hdl.handle.net/1721.1/81031</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">857790990</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, June 2013.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">"June 2013." Cataloged from PDF version of thesis.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Includes bibliographical references.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">Sexual reproduction depends on meiosis, the specialized cell division that gives rise to gametes. During meiosis, two consecutive rounds of chromosome segregation follow one round of DNA replication to yield four haploid gametes from one diploid progenitor. In meiosis I, homologous chromosomes segregate and in meiosis 11, sister chromatids split. Much of the same cell cycle machinery controls mitosis and meiosis. However, segregation of homologous chromosomes in meiosis I and progression into meiosis 11 directly after meiosis I necessitate several modifications to the basic cell cycle machinery. In this thesis, I have investigated how cell cycle regulators function during gametogenesis. First, I show that the mitotic exit network, which is a signaling pathway essential for mitotic exit, is dispensable for the meiotic divisions, and in fact signals via a mechanism distinct from mitosis. Second, I present data that the Polo kinase Cdc5, which activates mitotic exit in budding yeast, has gained additional roles during meiosis 1. I show that CDC5 is required for the removal of cohesin from chromosome arms in meiosis I, which is a prerequisite for meiosis I segregation. Despite the central role of CDC5 in regulating meiosis I, CDC5 is dispensable during meiosis 11. In sum, understanding how cell cycle regulators control the specialized meiotic divisions has improved our understanding of how different cell division types are established.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Michelle Andrea Attner.</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">265 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>
   <dim:field mdschema="dc" element="rights" lang="en_US">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.</dim:field>
   <dim:field mdschema="dc" element="rights" qualifier="uri" lang="en_US">http://dspace.mit.edu/handle/1721.1/7582</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">Biology.</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">Cell cycle regulation during gametogenesis in budding yeast</dim:field>
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   	&lt;Title>Cell cycle regulation during gametogenesis in budding yeast&lt;/Title>
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   	&lt;PublicationDate>2013&lt;/PublicationDate>
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        	&lt;DisplayName>Attner, Michelle Andrea&lt;/DisplayName>
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            &lt;DisplayName>Massachusetts Institute of Technology&lt;/DisplayName>
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    &lt;Keyword>Biology.&lt;/Keyword>
   	&lt;Abstract>Sexual reproduction depends on meiosis, the specialized cell division that gives rise to gametes. During meiosis, two consecutive rounds of chromosome segregation follow one round of DNA replication to yield four haploid gametes from one diploid progenitor. In meiosis I, homologous chromosomes segregate and in meiosis 11, sister chromatids split. Much of the same cell cycle machinery controls mitosis and meiosis. However, segregation of homologous chromosomes in meiosis I and progression into meiosis 11 directly after meiosis I necessitate several modifications to the basic cell cycle machinery. In this thesis, I have investigated how cell cycle regulators function during gametogenesis. First, I show that the mitotic exit network, which is a signaling pathway essential for mitotic exit, is dispensable for the meiotic divisions, and in fact signals via a mechanism distinct from mitosis. Second, I present data that the Polo kinase Cdc5, which activates mitotic exit in budding yeast, has gained additional roles during meiosis 1. I show that CDC5 is required for the removal of cohesin from chromosome arms in meiosis I, which is a prerequisite for meiosis I segregation. Despite the central role of CDC5 in regulating meiosis I, CDC5 is dispensable during meiosis 11. In sum, understanding how cell cycle regulators control the specialized meiotic divisions has improved our understanding of how different cell division types are established.&lt;/Abstract>
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