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A MTF2-Containing PRC2.1 Subcomplex Opposes G1 Progression Through Repressing CCND1 and CCND2 Transcription.
A MTF2-Containing PRC2.1 Subcomplex Opposes G1 Progression Through Repressing CCND1 and CCND2 Transcription.
상세정보
- 자료유형
- 학위논문
- Control Number
- 0017163556
- International Standard Book Number
- 9798384075639
- Dewey Decimal Classification Number
- 574
- Main Entry-Personal Name
- Longhurst, Adam.
- Publication, Distribution, etc. (Imprint
- [S.l.] : University of California, San Francisco., 2024
- Publication, Distribution, etc. (Imprint
- Ann Arbor : ProQuest Dissertations & Theses, 2024
- Physical Description
- 80 p.
- General Note
- Source: Dissertations Abstracts International, Volume: 86-03, Section: B.
- General Note
- Advisor: Madhani, Hiten.
- Dissertation Note
- Thesis (Ph.D.)--University of California, San Francisco, 2024.
- Summary, Etc.
- 요약Progression through the G1 phase of the cell cycle is the most highly regulated step in cellular division. We employed a chemogenetic approach to discover novel cellular networks that regulate cell cycle progression. This approach uncovered functional clusters of genes that altered sensitivity of cells to inhibitors of the G1/S transition. Mutation of components of the Polycomb Repressor Complex 2 rescued growth inhibition caused by the CDK4/6 inhibitor palbociclib, but not to inhibitors of S phase or mitosis. In addition to its core catalytic subunits, mutation of the PRC2.1 accessory protein MTF2, but not the PRC2.2 protein JARID2, rendered cells resistant to palbociclib treatment. We found that PRC2.1 (MTF2), but not PRC2.2 (JARID2), was critical for promoting H3K27me3 deposition at CpG islands genome-wide and in promoters. This included the CpG islands in the promoter of the CDK4/6 cyclins CCND1 and CCND2, and loss of MTF2 lead to upregulation of both CCND1 and CCND2. Our results demonstrate a role for PRC2.1, but not PRC2.2, in promoting G1 progression.
- Subject Added Entry-Topical Term
- Molecular biology.
- Subject Added Entry-Topical Term
- Cellular biology.
- Subject Added Entry-Topical Term
- Genetics.
- Subject Added Entry-Topical Term
- Biochemistry.
- Index Term-Uncontrolled
- Cell cycle
- Index Term-Uncontrolled
- Cyclin D
- Index Term-Uncontrolled
- Cyclin-dependent Kinase
- Index Term-Uncontrolled
- Palbociclib
- Index Term-Uncontrolled
- Polycomb Repressive Complex 2
- Added Entry-Corporate Name
- University of California, San Francisco Biochemistry and Molecular Biology
- Host Item Entry
- Dissertations Abstracts International. 86-03B.
- Electronic Location and Access
- 로그인을 한후 보실 수 있는 자료입니다.
- Control Number
- joongbu:655673
MARC
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■006m o d
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■020 ▼a9798384075639
■035 ▼a(MiAaPQ)AAI31489985
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aLonghurst, Adam.▼0(orcid)0000-0002-2463-8370
■24512▼aA MTF2-Containing PRC2.1 Subcomplex Opposes G1 Progression Through Repressing CCND1 and CCND2 Transcription.
■260 ▼a[S.l.]▼bUniversity of California, San Francisco. ▼c2024
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2024
■300 ▼a80 p.
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-03, Section: B.
■500 ▼aAdvisor: Madhani, Hiten.
■5021 ▼aThesis (Ph.D.)--University of California, San Francisco, 2024.
■520 ▼aProgression through the G1 phase of the cell cycle is the most highly regulated step in cellular division. We employed a chemogenetic approach to discover novel cellular networks that regulate cell cycle progression. This approach uncovered functional clusters of genes that altered sensitivity of cells to inhibitors of the G1/S transition. Mutation of components of the Polycomb Repressor Complex 2 rescued growth inhibition caused by the CDK4/6 inhibitor palbociclib, but not to inhibitors of S phase or mitosis. In addition to its core catalytic subunits, mutation of the PRC2.1 accessory protein MTF2, but not the PRC2.2 protein JARID2, rendered cells resistant to palbociclib treatment. We found that PRC2.1 (MTF2), but not PRC2.2 (JARID2), was critical for promoting H3K27me3 deposition at CpG islands genome-wide and in promoters. This included the CpG islands in the promoter of the CDK4/6 cyclins CCND1 and CCND2, and loss of MTF2 lead to upregulation of both CCND1 and CCND2. Our results demonstrate a role for PRC2.1, but not PRC2.2, in promoting G1 progression.
■590 ▼aSchool code: 0034.
■650 4▼aMolecular biology.
■650 4▼aCellular biology.
■650 4▼aGenetics.
■650 4▼aBiochemistry.
■653 ▼aCell cycle
■653 ▼aCyclin D
■653 ▼aCyclin-dependent Kinase
■653 ▼aPalbociclib
■653 ▼aPolycomb Repressive Complex 2
■690 ▼a0307
■690 ▼a0379
■690 ▼a0369
■690 ▼a0487
■71020▼aUniversity of California, San Francisco▼bBiochemistry and Molecular Biology.
■7730 ▼tDissertations Abstracts International▼g86-03B.
■790 ▼a0034
■791 ▼aPh.D.
■792 ▼a2024
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17163556▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
