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Regulation of Chromatin Structure and Segregation- [electronic resource]
Regulation of Chromatin Structure and Segregation- [electronic resource]
상세정보
- 자료유형
- 학위논문파일 국외
- 최종처리일시
- 20240214101701
- ISBN
- 9798380335997
- DDC
- 574
- 저자명
- Ng, Henry.
- 서명/저자
- Regulation of Chromatin Structure and Segregation - [electronic resource]
- 발행사항
- [S.l.]: : University of California, San Francisco., 2023
- 발행사항
- Ann Arbor : : ProQuest Dissertations & Theses,, 2023
- 형태사항
- 1 online resource(153 p.)
- 주기사항
- Source: Dissertations Abstracts International, Volume: 85-03, Section: B.
- 주기사항
- Advisor: Johnson, Alexander;Al-Sady, Bassem.
- 학위논문주기
- Thesis (Ph.D.)--University of California, San Francisco, 2023.
- 사용제한주기
- This item must not be sold to any third party vendors.
- 초록/해제
- 요약The genetic material is packaged differentially at different phases of the cell cycle. In interphase, cells package their genome into heterochromatin and euchromatin domains, where genes are repressed or expressed based on cell identity. Heterochromatin, the gene-repressive structure, is regulated by different factors that control methylation and acetylation on histones. During cell division, these histone modifications are copied onto the newly synthesized DNA. The heterochromatin structure is seeded from nucleation DNA sequence that recruits other factors to spread the domain. In our studies, we found that the factors required for spreading heterochromatin in different genomic regions are highly variable. Notably, we proposed a mechanism by which Fkh2, a transcription factor, recruits Clr6 histone deacetylase complex I" to a nucleated heterochromatin domain that initiates the spread of heterochromatin domains.During mitosis, the chromatin is packaged into condensed chromosomes for faithful segregation of the duplicated genome. Progression through mitosis is regulated by the levels of a family of protein kinase complexes named Cyclin-Dependent Kinases (CDKs). The phosphorylation of numerous CDK substrates drives various mitosis events. We identified a novel phosphate-binding pocket on cyclins that aids in the timing of sequential multisite phosphorylation in CDK substrates and mitotic events. Loss of this pocket causes a mitotic delay in vivo as well as loss of multisite phosphorylation in various CDK substrates in vitro.
- 일반주제명
- Biochemistry.
- 일반주제명
- Cellular biology.
- 일반주제명
- Genetics.
- 키워드
- Heterochromatin
- 키워드
- Mitosis
- 키워드
- Phosphorylation
- 키워드
- Cell cycle
- 키워드
- Genetic material
- 기타저자
- University of California, San Francisco Biochemistry and Molecular Biology
- 기본자료저록
- Dissertations Abstracts International. 85-03B.
- 기본자료저록
- Dissertation Abstract International
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
008240612s2023 us |||||||||||||||c||eng d■001000016934843
■00520240214101701
■006m o d
■007cr#unu||||||||
■020 ▼a9798380335997
■035 ▼a(MiAaPQ)AAI30635715
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aNg, Henry.▼0(orcid)0000-0002-6724-9607
■24510▼aRegulation of Chromatin Structure and Segregation▼h[electronic resource]
■260 ▼a[S.l.]:▼bUniversity of California, San Francisco. ▼c2023
■260 1▼aAnn Arbor :▼bProQuest Dissertations & Theses, ▼c2023
■300 ▼a1 online resource(153 p.)
■500 ▼aSource: Dissertations Abstracts International, Volume: 85-03, Section: B.
■500 ▼aAdvisor: Johnson, Alexander;Al-Sady, Bassem.
■5021 ▼aThesis (Ph.D.)--University of California, San Francisco, 2023.
■506 ▼aThis item must not be sold to any third party vendors.
■520 ▼aThe genetic material is packaged differentially at different phases of the cell cycle. In interphase, cells package their genome into heterochromatin and euchromatin domains, where genes are repressed or expressed based on cell identity. Heterochromatin, the gene-repressive structure, is regulated by different factors that control methylation and acetylation on histones. During cell division, these histone modifications are copied onto the newly synthesized DNA. The heterochromatin structure is seeded from nucleation DNA sequence that recruits other factors to spread the domain. In our studies, we found that the factors required for spreading heterochromatin in different genomic regions are highly variable. Notably, we proposed a mechanism by which Fkh2, a transcription factor, recruits Clr6 histone deacetylase complex I" to a nucleated heterochromatin domain that initiates the spread of heterochromatin domains.During mitosis, the chromatin is packaged into condensed chromosomes for faithful segregation of the duplicated genome. Progression through mitosis is regulated by the levels of a family of protein kinase complexes named Cyclin-Dependent Kinases (CDKs). The phosphorylation of numerous CDK substrates drives various mitosis events. We identified a novel phosphate-binding pocket on cyclins that aids in the timing of sequential multisite phosphorylation in CDK substrates and mitotic events. Loss of this pocket causes a mitotic delay in vivo as well as loss of multisite phosphorylation in various CDK substrates in vitro.
■590 ▼aSchool code: 0034.
■650 4▼aBiochemistry.
■650 4▼aCellular biology.
■650 4▼aGenetics.
■653 ▼aHeterochromatin
■653 ▼aMitosis
■653 ▼aPhosphorylation
■653 ▼aCell cycle
■653 ▼aGenetic material
■690 ▼a0487
■690 ▼a0379
■690 ▼a0369
■71020▼aUniversity of California, San Francisco▼bBiochemistry and Molecular Biology.
■7730 ▼tDissertations Abstracts International▼g85-03B.
■773 ▼tDissertation Abstract International
■790 ▼a0034
■791 ▼aPh.D.
■792 ▼a2023
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T16934843▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
■980 ▼a202402▼f2024
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