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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 서양
- 최종처리일시
- 20250211152723
- ISBN
- 9798384075639
- DDC
- 574
- 저자명
- Longhurst, Adam.
- 서명/저자
- A MTF2-Containing PRC2.1 Subcomplex Opposes G1 Progression Through Repressing CCND1 and CCND2 Transcription
- 발행사항
- [Sl] : University of California, San Francisco, 2024
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2024
- 형태사항
- 80 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-03, Section: B.
- 주기사항
- Advisor: Madhani, Hiten.
- 학위논문주기
- Thesis (Ph.D.)--University of California, San Francisco, 2024.
- 초록/해제
- 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.
- 일반주제명
- Molecular biology
- 일반주제명
- Cellular biology
- 일반주제명
- Genetics
- 일반주제명
- Biochemistry
- 키워드
- Cell cycle
- 키워드
- Cyclin D
- 키워드
- Palbociclib
- 기타저자
- University of California, San Francisco Biochemistry and Molecular Biology
- 기본자료저록
- Dissertations Abstracts International. 86-03B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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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[Sl]▼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.
