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Towards the understanding of CCNB1IP1 as a co-regulator of meiotic crossing-over in the mouse- [electronic resource]
Towards the understanding of CCNB1IP1 as a co-regulator of meiotic crossing-over in the mouse- [electronic resource]
상세정보
- 자료유형
- 학위논문(국외)
- 자관 청구기호
- 기본표목-개인명
- 표제와 책임표시사항
- Towards the understanding of CCNB1IP1 as a co-regulator of meiotic crossing-over in the mouse - [electronic resource] / Strong, Edward Remco.
- 발행, 배포, 간사 사항
- 발행, 배포, 간사 사항
- 형태사항
- 1 online resource(117 p)
- 일반주기
- Source: Dissertation Abstracts International, Volume: 75-06(E), Section: B.
- 일반주기
- Adviser: John Schimenti.
- 학위논문주기
- Thesis (Ph.D.)--Cornell University, 2014.
- 이용제한주기
- This item is not available from ProQuest Dissertations & Theses.
- 요약 등 주기
- 요약It is clear that there are many genes required for meiosis in mammals that are not present in the more tractable model organisms. To identify such genes, our lab has performed forward genetic chemical (ENU) mutagenesis screens for alleles conferring infertility in mice. A novel allele, Ccnb1ip1 mei4, generated in these screens is of interest because it is defective in a form of recombination called crossing-over. Ccnb1ip1 mei4/mei4 results in male and female infertility of otherwise normal-appearing animals.
- 요약 등 주기
- 요약CCNB1IP1 is finely regulated in both timing and localization to the events of meiotic crossover formations. Towards understanding the molecular functions of CCNB1IP1 and how the defect in Ccnb1ip1me4i/mei4 animals leads to meiotic arrest, studies of CCNB1IP1 within meiocytes implicate a role for CCNB1IP1 in SUMOylation. Remarkably little is understood about SUMO-modification consequences to meiosis. Protein-protein interactions with CCNB1IP1 identify a number of putative targets of SUMOylation, and subsequent in vivo biochemical interrogations reveal the CCNB1IP1-interacting proteins 4930455F23RIK and GGN as targets of posttranslational modification dependent upon a putative SUMO E3 ligase. In totality, these studies support the hypothesis that CCNB1IP1 performs as a meiotic co-regulator, mediating the SUMO-modification of proteins essential to the stabilization and maturation of crossover intermediates. These studies of CCNB1IP1 point towards a better understanding of meiosis, with emphasis upon new targets and roles of SUMOylation.
- 주제명부출표목-일반주제명
- 주제명부출표목-일반주제명
- 부출표목-단체명
- 기본자료저록
- Dissertation Abstracts International. 75-06B(E).
- 기본자료저록
- Dissertation Abstract International
- 전자적 위치 및 접속
- 원문정보보기
- 소장사항
-
20180515 2018
MARC
008180601s2014 us esm 001c eng■001MOKWON01257721
■00520180518094441
■007cr
■020 ▼a9781303749780
■035 ▼a(MiAaPQ)AAI3579158
■040 ▼aMiAaPQ▼cMiAaPQ
■090 ▼a전자도서(박사논문)
■1001 ▼aStrong, Edward Remco.
■24510▼aTowards the understanding of CCNB1IP1 as a co-regulator of meiotic crossing-over in the mouse▼h[electronic resource]▼cStrong, Edward Remco.
■260 ▼a[Sl]▼bCornell University▼c2014
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2014
■300 ▼a1 online resource(117 p)
■500 ▼aSource: Dissertation Abstracts International, Volume: 75-06(E), Section: B.
■500 ▼aAdviser: John Schimenti.
■5021 ▼aThesis (Ph.D.)--Cornell University, 2014.
■506 ▼aThis item is not available from ProQuest Dissertations & Theses.
■520 ▼aIt is clear that there are many genes required for meiosis in mammals that are not present in the more tractable model organisms. To identify such genes, our lab has performed forward genetic chemical (ENU) mutagenesis screens for alleles conferring infertility in mice. A novel allele, Ccnb1ip1 mei4, generated in these screens is of interest because it is defective in a form of recombination called crossing-over. Ccnb1ip1 mei4/mei4 results in male and female infertility of otherwise normal-appearing animals.
■520 ▼aCCNB1IP1 is finely regulated in both timing and localization to the events of meiotic crossover formations. Towards understanding the molecular functions of CCNB1IP1 and how the defect in Ccnb1ip1me4i/mei4 animals leads to meiotic arrest, studies of CCNB1IP1 within meiocytes implicate a role for CCNB1IP1 in SUMOylation. Remarkably little is understood about SUMO-modification consequences to meiosis. Protein-protein interactions with CCNB1IP1 identify a number of putative targets of SUMOylation, and subsequent in vivo biochemical interrogations reveal the CCNB1IP1-interacting proteins 4930455F23RIK and GGN as targets of posttranslational modification dependent upon a putative SUMO E3 ligase. In totality, these studies support the hypothesis that CCNB1IP1 performs as a meiotic co-regulator, mediating the SUMO-modification of proteins essential to the stabilization and maturation of crossover intermediates. These studies of CCNB1IP1 point towards a better understanding of meiosis, with emphasis upon new targets and roles of SUMOylation.
■590 ▼aSchool code: 0058.
■650 4▼aGenetics
■650 4▼aEvolution & development
■690 ▼a0369
■690 ▼a0412
■71020▼aCornell University▼bGenetics, Genomics, and Development.
■7730 ▼tDissertation Abstracts International▼g75-06B(E).
■773 ▼tDissertation Abstract International
■790 ▼a0058
■791 ▼aPh.D.
■792 ▼a2014
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T14824023▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
■980 ▼a20180515▼f2018
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