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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 鄧述諄(Shu-Chun Teng) | |
| dc.contributor.author | Zih-Jie Shen | en |
| dc.contributor.author | 沈子傑 | zh_TW |
| dc.date.accessioned | 2021-06-16T03:37:06Z | - |
| dc.date.available | 2020-09-25 | |
| dc.date.copyright | 2015-09-25 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-05-20 | |
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BioEssays : news and reviews in molecular, cellular and developmental biology 25, 856-867. Yaakov, G., Bell, M., Hohmann, S., and Engelberg, D. (2003). Combination of two activating mutations in one HOG1 gene forms hyperactive enzymes that induce growth arrest. Molecular and cellular biology 23, 4826-4840. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/54711 | - |
| dc.description.abstract | 在自然界中，細胞必須針對瞬息萬變的外在壓力做出快速並且適當的反應。當細胞遭遇環境壓力，例如滲透壓改變、養份缺乏、氧化壓力或是遺傳物質損害……等等的挑戰，細胞週期會停頓在G1時期，讓還未進入複製週期的細胞，能適應並且排除壓力，維持生存的能力。細胞週期中G1到S期的轉換大部份是靠G1週期素和Cdk1週期素依賴性蛋白激酶複合體的活性來調控。G1週期素中的Cln1和Cln2對於細胞週期的啟動提供了特殊的貢獻，而Cln3則是作用在CLN1和CLN2時間點上的表現和其他在G1時期表現的基因。之前的研究顯示出Ypl014w (我們命名為Sic2)是G1週期素/Cdk1複合體的其中一員。然而，這個基因是如何在細胞週期中被調控以及是否影響G1週期素–週期素依賴性蛋白激酶複合體的活性仍然是未知的。在本篇論文中，我們發現SIC2表現在壓力狀況下，由Mns2/4轉錄因子透過啟動子內STRE位置調控細胞週期中G1時期，經轉錄因子Mcm1的直接接合於啟動子內ECB位置調控。當Sic2大量表現時，細胞週期大規模地停滯在G1時期。除此之外，我們用共同免疫沉澱法證實了Sic2和G1週期素是會互相結合的，特別是Cln3的結合。在高滲透壓的情況下，Hog1 磷酸化酶會在Sic2上頭的T65，T69，T73做磷酸化修飾，而且這些磷酸化修飾有助於與G1週期素的結合。最後，Sic2對於滲透壓力造成的暫時性G1週期停頓有重要的貢獻，並在此壓力情況下與Sic1有重複性的功能。本篇論文證明Sic2可能是週期素依賴性蛋白激酶的抑制物，且在細胞遭受環境壓力時調控細胞週期的進行。 | zh_TW |
| dc.description.abstract | Cells require quick and proper response for the adaptive of various environmental changes. When cells encounter stresses such as osmotic stress, heat stress, nutrient depletion, oxidative stress, and DNA damage, cells arrest at G1 stage to provide proper adaptation and overcome stress challenge. The G1-S transition in the cell cycle is mainly regulated by the activity of the Cdk1/G1 cyclin-dependent protein kinase complex. Among G1 cyclins, Cln1 and Cln2 make specific contribution to the initiation of cell cycle, while Cln3 functions for the timely expression of CLN1, CLN2 and other G1-specific genes. Previous large scale analysis suggests that Sic2 is a component of the Cdk1/G1 cyclin complex. However, it is still elusive how SIC2 is cell cycle-regulated and whether it affects the activity of the Cdk1/G1 cyclin complex. Here we showed that SIC2 is expressed when cells encounter stresses. Its stress- and cell cycle-mediated expressions are driven by the transcriptional factors Msn2/4 and Mcm1, respectively. Sic2 overexpression caused cell cycle arrest at G1 stage. Co-immunoprecipitation experiments demonstrate a specific interaction between Sic2 and G1 cyclins, especially Cln3. Hog1 phosphorylates Sic2 at T65, T69 and T73 residues upon the osmotic stress, and these phosphorylations are essential for the association with Cln3. Sic2 is redundant to Sic1 under such condition which cause cells are arrested at G1 phase. Altogether, Sic2 may act as a CDK inhibitor to modulate cell cycle progression when cells encounter general stresses. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T03:37:06Z (GMT). No. of bitstreams: 1 ntu-104-D98445008-1.pdf: 2867018 bytes, checksum: f898253442736a19e6dccc01edaa2d88 (MD5) Previous issue date: 2015 | en |
| dc.description.tableofcontents | INTRODUCTION 1 MATERIALS METHODS 6 Yeast strains and plasmids 6 Cell synchronization and protein analysis 6 RNA analysis and Northern blot 7 Chromatin immunoprecipitation (ChIP) analysis 7 Reverse transcription and real-time PCR assay 8 Budding index under osmotic stress 8 RESULTS 9 Stress induce SIC2 expression 9 The expression of SIC2 under stresses is dependent on Msn2/4 9 The STRE elements are important for stress-induced SIC2 expression 10 Overexpression of Sic2 induces G1 arrest 11 SIC2 is expressed in G1 stage during the cell cycle 12 Mcm1 regulates SIC2 expression at the M/G1 junction 12 Sic2 is phosphorylated by Hog1 under osmotic stress 13 The association of Sic2 with Cln2 and Cln3 is regulated by Hog1 dependent phosphoylation 14 Sic2 is involved in osmotic stress induced transitory G1 delay 15 Sic2 regulates G1/S cell cycle progression by inhibiting Cdk1/Cln3 activity 16 DISCUSSION 18 FIGURES 21 REFERENCES 31 APPENDIX 43 | |
| dc.language.iso | en | |
| dc.subject | 週期素 | zh_TW |
| dc.subject | 磷酸化?抑制物 | zh_TW |
| dc.subject | 細胞週期 | zh_TW |
| dc.subject | 環境困境 | zh_TW |
| dc.subject | 磷酸化? | zh_TW |
| dc.subject | CKI | en |
| dc.subject | cyclins | en |
| dc.subject | Hog1 | en |
| dc.subject | environmental stresses | en |
| dc.subject | cell cycle | en |
| dc.title | Sic2 為一酵母菌困境誘導之細胞週期G1時期磷酸化酶抑制物 | zh_TW |
| dc.title | Sic2, a stress induced potential CKI, participates in G1 checkpoint in Saccharomyces cerevisiae | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 103-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 林敬哲(Jing-Jer Lin),李財坤(Tsai-Kun Li),詹迺立(Nei-Li Chan),鄭子豪(Tzu-Hao Cheng) | |
| dc.subject.keyword | 磷酸化?抑制物,細胞週期,環境困境,磷酸化?,週期素, | zh_TW |
| dc.subject.keyword | CKI,cell cycle,environmental stresses,Hog1,cyclins, | en |
| dc.relation.page | 53 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2015-05-20 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 微生物學研究所 | zh_TW |
| 顯示於系所單位： | 微生物學科所 | |
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