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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 鄧述諄(Shu-Chun Teng) | |
| dc.contributor.author | Chein-Wei Wang | en |
| dc.contributor.author | 王健瑋 | zh_TW |
| dc.date.accessioned | 2021-06-08T00:44:26Z | - |
| dc.date.copyright | 2015-09-25 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-08-06 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/17837 | - |
| dc.description.abstract | 為了在自然界中生存，酵母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。細胞當細胞遭遇環境壓力，例如滲透壓壓力時，細胞週期會停頓在G1時期，讓細胞適應並且排除壓力。細胞週期中G1到S期的轉換是由G1週期素和Cdc28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時間點之上的表現和其他在G1時期表現的基因。之前的研究顯示出Ypl014w (我們命名為Sic2)是Cdc28/G1週期素複合體的其中一員。然而，這個基因是如何在細胞週期中被調控，以及是否影響週期素依賴性蛋白激酶素–G1週期素複合體的活性仍然是未知的。在本篇論文中，我們發現SIC2會在細胞遭遇逆境時被轉錄因子Mns2/4表現，或是隨者細胞週期中受到轉錄因子Mcm1的調控。當Sic2大量表現時，細胞週期大規模地停滯在G1時期。利用共同免疫沉澱法證實了Sic2和G1週期素是會互相結合的。此外，Sic2對於滲透壓力造成的暫時性G1週期停頓有重要的貢獻，其功能在此逆境情況下與Sic1有重複性。本篇論文證明Sic2可能是週期素依賴性蛋白激酶的抑制物，且在細胞遭受逆境時調控細胞週期的進行。 | zh_TW |
| dc.description.abstract | To survive, budding yeast Saccharomyces cerevisiae delays G1 progression under several stresses, such as osmotic stress, to prevent damage accumulation. The G1-S transition is controlled by the activity of Cdk1/G1 cyclin. Proteomic screening suggested that Sic2 is a component of the Cdk1/G1 cyclin complex. However, the regulation of Sic2 expression or its functions on the activity of the Cdk1/G1 cycling complex is still unknown. Here we demonstrated that expression of Sic2 is not only regulated through stress mediated transcriptional factor Msn2/4, but also by cell cycle mediated transcriptional factor Mcm1. Overexpression of Sic2 causes cyclin-mediated-cell cycle arrest at G1 stage, and this cell cycle inhibition of Sic2 is dependent on osmotic stress-induced T65, T69, T73 and S192 phosphorylation. The phosphorylation of Sic2 is required for its Cln3 interaction, which may cause the reduction of Cdk1/Cln3 activity by the competition with the Cdk1-Cln3 interaction. Under osmotic stress, we found that Sic2 can cause transient G1 delay and play as a functional redundant protein of major stress-induced CKI, Sic1. Our study implies that Sic2 serves as a CDK inhibitor to modulate cell cycle progression under environmental stresses. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-08T00:44:26Z (GMT). No. of bitstreams: 1 ntu-104-R02445129-1.pdf: 1835213 bytes, checksum: 556926c921d45831debfd9cc16311b5b (MD5) Previous issue date: 2015 | en |
| dc.description.tableofcontents | INTRODUCTION 1 RESULTS 7 Stress induce SIC2 expression 7 The expression of SIC2 under stresses is dependent on Msn2/4 7 The STRE elements are important for stress-induced SIC2 expression 8 Overexpression of Sic2 induces G1 arrest 9 SIC2 is expressed in G1 stage during the cell cycle 10 Mcm1 regulates SIC2 expression at the M/G1 junction 11 Sic2 is phosphorylated under osmotic stress, and these phosphorylations facilitate cell cycle arrest 12 Sic2-S192 could be phosphorylated by Ypk2 13 Sic2-3T are phosphorylated by Hog1 under osmotic stress 14 The association of Sic2 with Cln2 and Cln3 is regulated by Hog1 dependent phosphorylation 15 Sic2 is involved in osmotic stress induced transitory G1 delay 17 Sic2 regulates G1/S cell cycle progression by inhibiting Cdk1/Cln3 activity 18 Sic2-Cln3 interaction is increased in Cdk1 interaction-defective cln3 mutants 20 sic2Δ mutant causes transitory effect in cell cycle timing 20 sic2Δ mutant does not affect genome instability 21 Discussion 22 MATERIALS METHODS 26 Yeast strains and plasmids 26 RNA analysis and Northern blot 27 Chromatin immunoprecipitation (ChIP) analysis 28 Reverse transcription and real-time PCR assay 28 Budding index under osmostress 29 Co- immunoprecipitation 29 Kinase prediction and screening 30 Phospo-specific antibody preparation 30 Phospho-protein detection 31 FIGURES 33 Contribution Table 54 REFERENCES 55 | |
| dc.language.iso | en | |
| dc.title | Sic2為一酵母菌逆境誘發之G1時期細胞週期磷酸酶抑制物 | 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 | 碩士 | |
| dc.contributor.oralexamcommittee | 林敬哲(Jing-Jer Lin),李財坤(Tsai-Kun Li) | |
| dc.subject.keyword | 細胞週期,逆境,磷酸?,週期素, | zh_TW |
| dc.subject.keyword | G1/S checkpoint,cyclin,kinase,stress, | en |
| dc.relation.page | 60 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2015-08-07 | |
| 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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