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Rudolf Jaenisch. Tudor, Matthew, 1973- Massachusetts Institute of Technology. Dept. of Biology. Massachusetts Institute of Technology. Department of Biology 2006-03-24T18:09:54Z 2006-03-24T18:09:54Z 2003 http://hdl.handle.net/1721.1/29993 54809089 Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2003. "September 2003." Includes bibliographical references. Cytosine-5-methylation has been associated with repression of transcription across eukaryotic phyla. In mammals, defects in methylation are associated with disease, developmental defects, and lethality. Furthermore, methylcytosine-specific binding proteins have been described which seem to effect the transcriptional repression associated with DNA methylation by modifying chromatin structure surrounding methylated sites. Whether these factors are, in fact, responsible for all of the essential functions of DNA methylation is unknown. We tested this possibility by creating mouse lines deficient for three factors shown to be methylcytosine-specific transcriptional repressors. Initial results suggest that these factors are not the only activities downstream of DNA methylation as their loss does not cause phenotypes as severe as loss of methylation. One of the factors studied, Mecp2 is the ortholog of the human gene mutated in Rett syndrome. Our deletion of Mecp2 in mice serves as a general model for the human disorder. Importantly, we find that transcription is not significantly deregulated in mice mutant for Mecp2, suggesting that the phenotypes seen are not a result of large-scale transcriptional derepression. by Matthew Tudor. Ph.D. 113 leaves 5635374 bytes 5635183 bytes application/pdf application/pdf eng Massachusetts Institute of Technology 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. http://dspace.mit.edu/handle/1721.1/7582 Biology. Genetic characterization of a family of mouse 5-methylcytosine binding protein genes Thesis application/pdf false Publication unknown unknown <Publication xmlns="https://www.openaire.eu/cerif-profile/1.1/" id="f0436107-2afb-4aed-a2a5-213a4c882865"> <Type xmlns="https://www.openaire.eu/cerif-profile/vocab/COAR_Publication_Types">http://purl.org/coar/resource_type/c_1843</Type> <Language>eng</Language> <Title>Genetic characterization of a family of mouse 5-methylcytosine binding protein genes</Title> <PublishedIn> <Publication> </Publication> </PublishedIn> <PublicationDate>2003</PublicationDate> <Authors> <Author> <DisplayName>Tudor, Matthew, 1973-</DisplayName> <Affiliation> <OrgUnit> </OrgUnit> </Affiliation> </Author> </Authors> <Editors> </Editors> <Publishers> <Publisher> <DisplayName>Massachusetts Institute of Technology</DisplayName> <OrgUnit /> </Publisher> </Publishers> <License>http://dspace.mit.edu/handle/1721.1/7582</License> <Keyword>Biology.</Keyword> <Abstract>Cytosine-5-methylation has been associated with repression of transcription across eukaryotic phyla. In mammals, defects in methylation are associated with disease, developmental defects, and lethality. Furthermore, methylcytosine-specific binding proteins have been described which seem to effect the transcriptional repression associated with DNA methylation by modifying chromatin structure surrounding methylated sites. Whether these factors are, in fact, responsible for all of the essential functions of DNA methylation is unknown. We tested this possibility by creating mouse lines deficient for three factors shown to be methylcytosine-specific transcriptional repressors. Initial results suggest that these factors are not the only activities downstream of DNA methylation as their loss does not cause phenotypes as severe as loss of methylation. One of the factors studied, Mecp2 is the ortholog of the human gene mutated in Rett syndrome. Our deletion of Mecp2 in mice serves as a general model for the human disorder. Importantly, we find that transcription is not significantly deregulated in mice mutant for Mecp2, suggesting that the phenotypes seen are not a result of large-scale transcriptional derepression.</Abstract> <Access xmlns="http://purl.org/coar/access_right" > </Access> </Publication>