<?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>2026-09-19T20:48:34Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/31183" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/31183</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">Seshan, Anupama</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">2006-02-02T18:56:29Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2006-02-02T18:56:29Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="copyright" lang="en_US">2005</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="issued" lang="en_US">2005</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="uri">http://hdl.handle.net/1721.1/31183</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">61270687</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2005.</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">The regulation of eukaryotic cell division, which involves the faithful segregation of a complete DNA complement to each daughter cell, is a fundamental area of research in biology. Entry into mitosis is initiated by the action of mitotic cyclins complexed with the cyclin dependent kinase (CDK). Once the chromosomes have been successfully segregated, the exit from mitosis ensues. In order for cells to exit from mitosis, mitotic CDKs must be inactivated. The inactivation of mitotic CDKs, in turn, promotes cytokinesis. In S. cerevisiae, mitotic exit is controlled by the Mitotic Exit Network (MEN). In this simple eukaryote, the tight coupling of nuclear migration and mitotic exit is achieved in part by the spatial segregation of Lte1, a positive activator of the MEN, and Teml, a GTPase that acts at the top of the MEN signaling cascade. The spatial segregation of Lte1 and Teml is particularly important in cells with mispositioned anaphase spindles, and plays a role in the prevention of aneuploidy. A model for the regulation of Lte1 localization across the cell cycle is proposed. Additionally, the role of Lte1 localization in mediating its ability to promote mitotic exit is examined. This work identifies novel connections between polarity determinants, Ras signaling, and mitotic exit.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">Anupama Seshan.</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">160 leaves</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="extent">8203312 bytes</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="extent">8225363 bytes</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="mimetype">application/pdf</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="mimetype">application/pdf</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">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">Regulation of the localization of Lte1, a S. cerevisiae mitotic exit activator</dim:field>
   <dim:field mdschema="dc" element="title" qualifier="alternative" lang="en_US">Understanding the regulation of the localization of Lte1, a S. cerevisiae mitotic exit activator</dim:field>
   <dim:field mdschema="dc" element="type" lang="en_US">Thesis</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="mimetype">application/pdf</dim:field>
   <dim:field mdschema="dspace" element="entity" qualifier="type">Publication</dim:field>
   <dim:field mdschema="others" element="access-status">unknown</dim:field>
   <dim:field mdschema="others" element="access-status">unknown</dim:field>
   <dim:field mdschema="cerif" element="openaire" authority="" confidence="-1">&lt;Publication xmlns="https://www.openaire.eu/cerif-profile/1.1/" id="9b1a2429-a4ca-4b7b-b732-fde59122c1df">
	&lt;Type xmlns="https://www.openaire.eu/cerif-profile/vocab/COAR_Publication_Types">http://purl.org/coar/resource_type/c_1843&lt;/Type>
	&lt;Language>eng&lt;/Language>
   	&lt;Title>Regulation of the localization of Lte1, a S. cerevisiae mitotic exit activator&lt;/Title>
   	&lt;Subtitle>Understanding the regulation of the localization of Lte1, a S. cerevisiae mitotic exit activator&lt;/Subtitle>
   	&lt;PublishedIn>
    	&lt;Publication>
      	&lt;/Publication>
   	&lt;/PublishedIn>
   	&lt;PublicationDate>2005&lt;/PublicationDate>
   	&lt;Authors>
      	&lt;Author>
        	&lt;DisplayName>Seshan, Anupama&lt;/DisplayName>
         	&lt;Affiliation>
         		&lt;OrgUnit>
         		&lt;/OrgUnit>
         	&lt;/Affiliation>
      	&lt;/Author>
	&lt;/Authors>
   	&lt;Editors>
	&lt;/Editors>
    &lt;Publishers>
        &lt;Publisher>
            &lt;DisplayName>Massachusetts Institute of Technology&lt;/DisplayName>
            &lt;OrgUnit />
        &lt;/Publisher>
    &lt;/Publishers>
    &lt;License&gt;http://dspace.mit.edu/handle/1721.1/7582&lt;/License>
    &lt;Keyword>Biology.&lt;/Keyword>
   	&lt;Abstract>The regulation of eukaryotic cell division, which involves the faithful segregation of a complete DNA complement to each daughter cell, is a fundamental area of research in biology. Entry into mitosis is initiated by the action of mitotic cyclins complexed with the cyclin dependent kinase (CDK). Once the chromosomes have been successfully segregated, the exit from mitosis ensues. In order for cells to exit from mitosis, mitotic CDKs must be inactivated. The inactivation of mitotic CDKs, in turn, promotes cytokinesis. In S. cerevisiae, mitotic exit is controlled by the Mitotic Exit Network (MEN). In this simple eukaryote, the tight coupling of nuclear migration and mitotic exit is achieved in part by the spatial segregation of Lte1, a positive activator of the MEN, and Teml, a GTPase that acts at the top of the MEN signaling cascade. The spatial segregation of Lte1 and Teml is particularly important in cells with mispositioned anaphase spindles, and plays a role in the prevention of aneuploidy. A model for the regulation of Lte1 localization across the cell cycle is proposed. Additionally, the role of Lte1 localization in mediating its ability to promote mitotic exit is examined. This work identifies novel connections between polarity determinants, Ras signaling, and mitotic exit.&lt;/Abstract>
	&lt;Access xmlns="http://purl.org/coar/access_right" 
    >
    &lt;/Access>
&lt;/Publication>
</dim:field>
</dim:dim>
</metadata></record></GetRecord></OAI-PMH>