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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 吳益群 | |
| dc.contributor.author | Chang-Yen Lee | en |
| dc.contributor.author | 李長晏 | zh_TW |
| dc.date.accessioned | 2021-06-15T05:03:59Z | - |
| dc.date.available | 2016-08-19 | |
| dc.date.copyright | 2011-08-19 | |
| dc.date.issued | 2011 | |
| dc.date.submitted | 2011-08-18 | |
| dc.identifier.citation | Andrabi, S.A., Kim, N.S., Yu, S.W., Wang, H., Koh, D.W., Sasaki, M., Klaus, J.A., Otsuka, T., Zhang, Z., Koehler, R.C., et al. (2006). Poly(ADP-ribose) (PAR) polymer is a death signal. Proc Natl Acad Sci U S A 103, 18308-18313.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/46331 | - |
| dc.description.abstract | Apoptosis is an evolutionarily conserved program of developmental cell death. During the development of the Caenorhabditis elegans hermaphrodite, 131 of the 1030 somatic cells acquire cell death fate and finally undergo apoptosis. The process of programmed cell death can be divided into four distinct steps: decision, execution, engulfment and degradation. The essential four players of the execution step consist of egl-1(BH3-only), ced-9(BCL-2), ced-4(APAF-1) and ced-3(Caspases). It has been shown that transcriptional activation of egl-1 occurs in some destined cell to die. EGL-1 promotes cell death by antagonizing the cell-death inhibitory function of CED-9, thereby allowing pro-apoptotic CED-4 interacts with CED-3 caspase, which in turn results in destruction of the cell. However, how the expression level of egl-1 is regulated and the identities of CED-3 substrates are largely unknown. Previous studies showed that the double mutations of grp-1(The C. elegans ortholog of the cytohesin family of ARF GEFs functions in signaling cells to control asymmetric neuroblast divisions) and pro-apoptotic genes but not single mutations result in abnormal tail morphology. Therefore, we undertook a genetic enhancer screen for novel pro-apoptotic genes in the grp-1 background. Here we report the characterization of two mutants, tp189 and tp71 isolated from the screen. Single nucleotide polymorphism (SNP) mapping was used to position tp189 to the right arm of linkage group IV. We then used deficiency mapping to map tp189 to a 0.5c.m. interval containing approximately 200 genes on 50 fosmids. Finally, we rescued the abnormal tail-defect of tp189 with fosmid WRM064aB04 containing 13 candidate genes including pme-3. tp189 fails to complement a pme-3 allele, suggesting that tp189 may have a mutation in the pme-3 gene. We also used the SNP method to define the other mutation tp71 between pkP2150 and CE2-244 on LG II. However, the tp71 tail-defect phenotype is independent of grp-1. We conclude that tp71 probably functions in hermaphrodite tail tip morphogenesis. In addition to the forward genetic approach, we simultaneously utilized a reverse genetic approach to identify a kinase gene kin-2 that may act together with src kinase, csk-1 to regulate programmed cell death. Our data shown that kin-2, a regulatory subunit of a cAMP-dependent protein kinase may have pro-apoptotic function. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T05:03:59Z (GMT). No. of bitstreams: 1 ntu-100-R98b43018-1.pdf: 2220957 bytes, checksum: 04ad789e4d0e0085dfd8541b7d5120fc (MD5) Previous issue date: 2011 | en |
| dc.description.tableofcontents | Table of Contents
口試委員會審定書 i DEDICATION ii 中文摘要 iii ABSTRACT v INTRODUCTION 1 MATERIALS AND METHODS 8 C. elegans Genetics 8 Test of dependence on grp-1(gm350) 9 Mapping the mutation in the tp189 recessive mutant and Complementation test 9 RNAi 10 RESULTS 11 Part I 11 tp189 has defects in hermaphrodite tail morphogenesis 11 The tp189 tail-defect phenotype depends on grp-1 12 Genetic mapping and molecular strategy of tp189 12 tp189 fails to complement pme-3 13 tp189 does not have extra touch neurons 14 Part II 15 tp71 also has defects in hermaphrodite tail morphogenesis 15 The tp71 tail-defect phenotype is independent of grp-1 15 Genetic mapping of tp71 16 The RNAi treatment of candidate genes in the region between pkP2150 and CE2-244 16 Part III 18 Mutation in kin-2 enhance extra cell number in weak ced-3 mutant 18 Expression of kin-2 in touch neurons kills touch neurons 18 DISCUSSION 20 REFERENCES 23 TABLES and FIGURES 31 Table 1. tp189 partially fails to complement pme-3(gk120). 31 Table 2. tp189 does not have extra touch neurons 32 Table 3. Phenotype of tp71 is independent of grp-1. 33 Table 4. RNAi of a few gene in the mapping region caused abnormal tail morphology. 34 Table 5. Mutation in kin-2 enhances extra cell number in weak ced-3 mutant. 35 Table 6. Expression of kin-2 in PLMs kills PLMs. 36 Figure 1. Interactions between grp-1 and ced-3 result in extra hypodermal cell(s). 37 Figure 2. grp-1 (gm350); tp189 mutants have tail morphological abnormalities. 38 Figure 3. grp-1 (gm350); tp189 results in morphologic defects in hyp10 or hyp11 of tail tip. 39 Figure 4. grp-1 (gm350); tp189 results in abnormal cellular arrangement of hyp9 and hyp10 in tail tip. 40 Figure 5. The tp189 tail-defect phenotype is dependent on grp-1(gm350). 41 Figure 6. Mapping interval can be defined on LG IV between 0.07 and 6.72 c.m.. 42 Figure 7. eDf18 fails to complement grp-1 (gm350); tp189. eDf18 stands for a deletion region of LG IV:3.64-4.27 c.m.. 43 Figure 8. grp-1 (gm350); tp189 can be rescue by fosmid WRM064aB04 and pme-3 gDNA. 44 Figure 9. The phenotype of grp-1(gm350); tp189 is similar to grp-1(gm350); pme-3(gk120). 45 Figure 10. tp71 mutants have tail morphological abnormalities. 46 Figure 11. tp71 results in morphologic defects in hyp9 and hyp10 of tail tip. 47 Figure 12. tp71 results in abnormal cellular arrangement of hyp9 and hyp10 in tail tip. 48 Figure 13. Mapping interval can be defined on LG II between -1.79 and 3.34 c.m.. 49 Figure 14. Mapping interval can be defined on LG II between 0.50 and 0.506 c.m.. 50 | |
| dc.language.iso | en | |
| dc.subject | 聚(腺 | zh_TW |
| dc.subject | 鳥嘌呤核 | zh_TW |
| dc.subject | 細胞凋亡 | zh_TW |
| dc.subject | 線蟲 | zh_TW |
| dc.subject | execution | en |
| dc.subject | kin-2 | en |
| dc.subject | pme-3 | en |
| dc.subject | C.elegans | en |
| dc.subject | apoptosis | en |
| dc.subject | grp-1 | en |
| dc.title | 描繪在計畫性細胞死亡和尾部型態中有缺陷線蟲突變株的特性 | zh_TW |
| dc.title | Characterization of C. elegans mutants defective in apoptosis and tail morphogenesis | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 99-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 李士傑,黃偉邦 | |
| dc.subject.keyword | 線蟲,細胞凋亡,鳥嘌呤核,聚(腺, | zh_TW |
| dc.subject.keyword | C.elegans,apoptosis,execution,grp-1,pme-3,kin-2, | en |
| dc.relation.page | 50 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2011-08-18 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 分子與細胞生物學研究所 | zh_TW |
| 顯示於系所單位： | 分子與細胞生物學研究所 | |
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