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Crosstalk of light signaling and unfolded protein response in Arabidopsis 원문보기

  • 저자

    푼야키 마이밤

  • 학위수여기관

    경상대학교 대학원

  • 학위구분

    국내박사

  • 학과

    응용생명과학부

  • 지도교수

  • 발행년도

    2014

  • 총페이지

    xiv, 96 p.

  • 키워드

    Relationship of light and ER stress in Arabidopsis;

  • 언어

    eng

  • 원문 URL

    http://www.riss.kr/link?id=T13534184&outLink=K  

  • 초록

    The protein folding in the ER is a very sensitive to various biotic or abiotic stress conditions which causes ER stress resulting in induction of a set of molecular chaperones to alleviate stress called the unfolded protein response. Light is required for maximal induction of UPR, but exactly how it regulates the process at the molecular level is still unknown. Light affects every aspect of plant development, beginning with seed germination till the seed maturation. In the absence of light, the seedlings undergo etiolation which is characterized by long hypocotyl, an apical hook and an unopened cotyledon. Once the seedling perceives sufficient light, it will deetiolate where the seedlings develop inhibition of hypocotyl growth, the apical hook opens, cotyledons expand, chloroplasts develop, and a new gene expression program is induced. These light signals can be perceived by different photoreceptors present in plants and modulate different physiological responses. Phytochromes regulate the expression of several downstream genes like HY5, which is key regulator of photomorphogenesis, is regulated by the E3 ubiquitin ligase COP1, a crucial repressor of light signaling. Apart from growth and development, light imparts fitness to plants by integrating the signalling from different abiotic stress condition in particular heat stress, cold stress and ROS stress. Different light signalling components like photoreceptors and downstream targets like COP1 and HY5 are involved in the integration of these responses. Moreover, the different abiotic stress conditions impair the ER homeostasis, which results in the accumulation of misfolded proteins in ER and cause the ER stress in cells. UPR is activated to mitigate the ER stress in plants The UPR responses play an important role to decrease misfolded/unfolded protein in the ER lumen. This pathway activates the regulation of protein translation and the production of chaperone proteins which assist protein folding. If the misfolded proteins still persist it leads to apoptosis. In this study it was found that light is required for the ER stress effect and increasing light intensity enhances sensitivity towards the ER stress. Also, the negative light signaling regulator cop1-4 mutant is sensitive while positive regulator hy5 mutant is tolerant to ER stress, which suggests the involvement in UPR signalling pathways. Furthermore, the expression levels and patterns of the UPR genes is higher in hy5 mutant as compared to WT under ER stress condition indicating that HY5 acts as a negative regulator for the UPR genes. HY5 binds to different light response elements like G-box. Also, bZIP28 binds to the ERSE I and ERSE II and up regulates the expression of ER stress induced-genes. Interestingly, the core motif of G-box (CGTG) is similar to the ERSE I (CGTGTC) and ERSE II (CACGTG). Thus, it was confirmed by in vitro and in vivo experiments that HY5 can bind to the UPR genes through ERSE elements while bZIP28 can bind to the light responsive genes through the G-box. BIP3 promoter contains ERSE I have the consensus promoter sequence CCAAT-N9-CCACG and ERSE II having the consensus sequence ATTGG-N9- CCACG. The CCAAT is the binding site for the NFY complexes whereas CCACG is the binding site of bZIP28. Thus, HY5 shares the common motif with bZIP28 for binding to the BIP3 promoter. Interestingly, HY5 can also compete with bZIP28 for binding to the BIP3 promoter in a concentration dependent manner. Also, HY5 interacts with bZIP28 and coregulate the target genes for expression through common cis elements. It also found that both HY5 and bZIP28 genetically interact with each other to regulate the crosstalk between light signalling and UPR. The sensitive phenotype of bzip28 can be rescued by the double mutant bzip28 hy5 partially. Interestingly, both HY5 and bZIP28 plays antagonistic role in gene expression of UPR genes and light responsive gene. HY5 acts as a negative regulator of the UPR responsive genes, while bZIP28 acts a negative regulator for the light responsive genes, suggesting that both act together to fine-tune each other expression. Inhibition of light responsive genes under ER stress by bZIP28 plays an important role for survival of plant under stress condition. Light also can be measured by measuring the hypocotyl growth. It was further confirmed that light signalling is impaired in the hy5 mutant as shown by the increase in hypocotyl length as compared with the WT whereas the light signalling is enhanced in bzip28 mutant as shown by more hypocotyl growth inhibition under ER stress conditions which confirms that light signaling is impaired by bZIP28 under ER stress condition. With the following results and data support that under unstressful condition HY5 associates with the ERSE elements and maintain the basal level of UPR genes. In the presence of ER stress, the bZIP28 accumulates with the ERSE elements and upregulate the expression of UPR genes which is important for the tolerant phenotype of the hy5. Our findings indicate the molecular mechanism involving the crosstalk of light and the UPR signaling through HY5 and bZIP28 transcription factor.


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