<?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>2026-09-19T05:15:09Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/57564" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/57564</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">Gerald R. Fink.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Wu, Chia-Yung</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">2010-08-26T15:28:47Z</dim:field>
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   <dim:field mdschema="dc" element="date" qualifier="copyright" lang="en_US">2010</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="issued" lang="en_US">2010</dim:field>
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   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">654417420</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>
   <dim:field mdschema="dc" element="description" lang="en_US">Cataloged from student submitted 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">Polyploidy, increased copy number of whole chromosome sets in the genome, is a common cellular state in evolution, development and disease. Polyploidy enlarges cell size and alters gene expression, producing novel phenotypes and functions. Although many polyploid cell types have been discovered, it is not clear how polyploidy changes physiology. Specifically, whether the enlarged cell size of polyploids causes differential gene regulation has not been investigated. In this thesis, I present the evidence for a size-sensing mechanism that alters gene expression in yeast. My results indicate a causal relationship between cell size and gene expression. Ploidy-associated changes in the transcriptome therefore reflect transcriptional adjustment to a larger cell size. The causal and regulatory connection between cell size and transcription suggests that the physical features of a cell (such as size and shape) are a systematic factor in gene regulation. In addition, cell size homeostasis may have a critical function - maintenance of transcriptional homeostasis.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Chia-Yung Wu.</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">127 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 
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   <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">Control of gene expression by cell size</dim:field>
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   	&lt;Title>Control of gene expression by cell size&lt;/Title>
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   	&lt;PublicationDate>2010&lt;/PublicationDate>
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    &lt;Keyword>Biology.&lt;/Keyword>
   	&lt;Abstract>Polyploidy, increased copy number of whole chromosome sets in the genome, is a common cellular state in evolution, development and disease. Polyploidy enlarges cell size and alters gene expression, producing novel phenotypes and functions. Although many polyploid cell types have been discovered, it is not clear how polyploidy changes physiology. Specifically, whether the enlarged cell size of polyploids causes differential gene regulation has not been investigated. In this thesis, I present the evidence for a size-sensing mechanism that alters gene expression in yeast. My results indicate a causal relationship between cell size and gene expression. Ploidy-associated changes in the transcriptome therefore reflect transcriptional adjustment to a larger cell size. The causal and regulatory connection between cell size and transcription suggests that the physical features of a cell (such as size and shape) are a systematic factor in gene regulation. In addition, cell size homeostasis may have a critical function - maintenance of transcriptional homeostasis.&lt;/Abstract>
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