cyclic-di-GMP가 H-NS와 Lon을 통해 살모넬라의 병원성관련 유전자들의 발현을 저해시킨다는 내용의 연구
DC Field | Value | Language |
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dc.contributor.advisor | 윤현진 | - |
dc.contributor.author | 정지수 | - |
dc.date.accessioned | 2019-08-13T16:40:55Z | - |
dc.date.available | 2019-08-13T16:40:55Z | - |
dc.date.issued | 2019-08 | - |
dc.identifier.other | 29352 | - |
dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/15492 | - |
dc.description | 학위논문(석사)--아주대학교 일반대학원 :분자과학기술학과,2019. 8 | - |
dc.description.tableofcontents | CONTENTS ABSTRACT...………………………………………………………...ⅰ LIST OF TABLES.......……………………………………………...ⅳ LIST OF FIGURES ……………………………………………........ⅴ 1. Introduction……………………………………………………... 1 2. Materials and Methods…………………………………………. 5 2.1 Bacterial growth condition…………………………………….... 5 2.2 Construction of bacterial strains……………………………........ 8 2.3 Construction of plasmids………………………………………... 8 2.4 Biofilm assay …………………………………………………... 13 2.5 Rdar morphotyping and calcofluor white staining ……….......... 13 2.6 Invasion assay ………………………………………………...... 13 2.7 RNA extraction ..………………………………………………. 14 2.8 Quantitative real-time PCR analysis…………………………… 14 2.9 SDS-PAGE and Western blot analysis..………………………… 15 3. Results 3.1 Overexpression of AdrA in Salmonella negatively controls the transcription of SPI-1 genes………………………………......16 3.2 Overexpression of AdrA in Salmonella is indeed defective for HilD-dependent expression of SPI-1 genes ………………………21 3.3 Overexpression of the AdrA no effect on HilD upstream regulatory gene in the transcription level…………………………………....24 3.4 Overexpression of the AdrA affects level of HilD protein mediated H-NS silencing…………………………………………………...30 3.5 Overexpression of the AdrA decrease level of HilD proteins using Lon protease……………………………………………………...34 4. Discussions………………………………………………………36 5. Reference ………………………………………………………..39 6. Abstract in Korean.......................................................................45 | - |
dc.language.iso | eng | - |
dc.publisher | The Graduate School, Ajou University | - |
dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
dc.title | cyclic-di-GMP가 H-NS와 Lon을 통해 살모넬라의 병원성관련 유전자들의 발현을 저해시킨다는 내용의 연구 | - |
dc.title.alternative | Jisu Jeong | - |
dc.type | Thesis | - |
dc.contributor.affiliation | 아주대학교 일반대학원 | - |
dc.contributor.alternativeName | Jisu Jeong | - |
dc.contributor.department | 일반대학원 분자과학기술학과 | - |
dc.date.awarded | 2019. 8 | - |
dc.description.degree | Master | - |
dc.identifier.localId | 952023 | - |
dc.identifier.uci | I804:41038-000000029352 | - |
dc.identifier.url | http://dcoll.ajou.ac.kr:9080/dcollection/common/orgView/000000029352 | - |
dc.description.alternativeAbstract | Salmonella enterica serovar Typhimurium injects a set of effector proteins into the cytoplasm of host cells via Salmonella pathogenicity island 1 (SPI-1) type III secretion system (T3SS) and induces bacterial invasion into host cells. Cyclic-di-GMP, a circular RNA dinucleotide synthesized by diguanylate cyclases, functions as a second messenger in a variety of physiological processes, including motility, biofilm formation, and virulence factor production. In this study, in order to address how cyclic-di-GMP regulates virulence factor production in S. Typhimurium, the role of cyclic-di-GMP in SPI-1 regulation was investigated. Overexpression of a diguanylate cyclase AdrA significantly decreased the mRNA expression and protein production of HilD, a master regulator of SPI-1, thereby down-regulating the expression of cognate SPI-1 genes. However, the negative regulation of SPI-1 by cyclic-di-GMP was abolished in the absence of H-NS or Lon, which represses hilD expression and controls HilD turnover, respectively. Considering that AdrA overexpression did not influence hns and lon expression, cyclic-di-GMP might exert negative regulation on SPI-1 by modulating the activity of H-NS and Lon. With regard to a pivotal role of cyclic-di-GMP in controlling motile and sessile lifestyles in diverse bacterial pathogens, this study suggests a new role of cyclic-di-GMP in Salmonella lifestyle conversion between colonization in intestinal lumen and invasion into host cells | - |
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