阿拉伯芥HIT4及HSP40蛋白質保護植物耐受高溫逆境之研究;Explores of the protecting mechanisms of Arabidopsis thaliana HIT4 and HSP40 against high temperature stress

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題名:	阿拉伯芥HIT4及HSP40蛋白質保護植物耐受高溫逆境之研究;Explores of the protecting mechanisms of Arabidopsis thaliana HIT4 and HSP40 against high temperature stress
作者:	羅予苡;Lo, Yu-Yi
貢獻者:	生命科學系
關鍵詞:	高溫逆境;表觀遺傳;染色質重塑;染色質中心;不完全顯性;熱休克蛋白;Heat stress;Epigenetic;Chromatin remodeling;Chromocenter;incompletely-dominant;Heat shock protien
日期:	2020-11-30
上傳時間:	2021-03-18 16:50:13 (UTC+8)
出版者:	國立中央大學
摘要:	植物為固著型生物，是以植物演化出許多適應及抵禦環境逆境的策略，避免受其傷害。由於溫室效應，全球暖化的關係，高溫逆境成為近年來嚴重影響作物產量的重要原因之一，因此如何提高植物耐受逆境已成為重要的課題。本實驗室先前利用前向式遺傳學研究法 (forward genetic approach)篩選到一棵對持續性熱逆境及熱休克逆境敏感的突變株 heat intolerant 4 (hit4)。後續研究發現， HIT4所編碼的產物位在染色質中心上。在植物遭受熱逆境時， HIT4會藉由染色質構型重塑，誘使染色質中心呈現消散狀態，促使平時靜默不轉錄 (transcriptional gene silencing, TGS)的基因活化，協助植物耐受高溫逆境。為了更進一步了解 HIT4耐熱的相關機制，本研究從 hit4突變植物篩選出能耐受持續性高溫的逆轉突變株 (hit4 命名為 revertant98 13 (r98 13)。接著以基因定位的方式，欲找尋使 hit4不耐熱性狀逆轉的突變基因。研究結果顯示， r98 13突變基因位於阿拉伯芥第二條色體底部。此外，為了瞭解參與 HIT4調節染色質中心凝縮或消散的其他因子，本研究也從 HIT4 GFP轉植株挑選出染色質中心數目異於野生型植株的突變株，命名為 18 18 2。 18 18 2具有晚花及雄配子異常的性狀。另一方面，本實驗室先前有篩到一棵對持續性熱逆境敏感但耐受熱休克逆性的突變株 hit intolerant 5( 其突變位置坐落於蛋白質法尼脂轉移? (PFT)之 β次單元基因上。阿拉伯芥家族 HSP40中的 J2及 J3已經被證實為 PFT的受質蛋白。 J2與 J3的胺基酸序列有高達 90%的相同度 (identity)，但只有 j3剔除突變株與 hit5有相同的熱反應性狀，且與 J3無法被法尼脂化之轉植株亦同，證實 J3法尼脂化與否會影響植物對熱逆境的耐受程度。本研究進一步證實法尼脂化對 HSP40與其他 HSPs間交互作用所產生的影響，及釐清 J2、 J3在熱逆境下分別扮演的角色。;Given that plants are immobile, their growth and development will be hampered seriously if environmental conditions are not suitable for their growth and development. High temperature is one of the abiotic stresses. In order to understand how plants to cope with high temperature stress, we used a forward genetic approach to isolate a heat sensitive mutant of the Arabidopsis named heat intolerant 4 (hit4). The hit4 mutant is sensitive to both prolonged heat stress and sudden heat shock treatment. The role of HIT4 was suggested to bring to date unidentified moleculars away from chromocenter thus allowing heat induced chromocenter decondensation to occur. To understand more about which molecular involved in these heat triggered HIT4 dependent responses, we isolated a revertants of hit4 named revertant 98 13 (r98 13), that restored the ability to tolerate prolonged heat stress like wild type. By map based cloning method, r98 13 mutated locus was shown to locate at a region between AGI map 19,628 kb~19,674 kb of the chromosome II. Meanwhile, we isolated a mutant, named as 18 18 2, whose number of chromocenter is different from that of wild type. The phenotype of 18 18 2 included delayed flowering and abnormal stamen. In addition, we have previously isolated the hit intolerant 5 (hit5) mutant. Incubation at 37°C for 4 days was lethal for hit5 but not for wild type plants. HIT5 encodes the β subunit of protein farnesyl transferase (PFT). Two of the Arabidopsis HSP40 homologs, AtJ2 (J2) and AtJ3 (J3), are PFT substrates. Although J2 and J3 have 90% amino acid sequences identitly, only j3 show the same heat stress phenotypes as hit5. Blocking the farnesylation of J3 in plants also show the same heat stress phenotypes as hit5. These results indicated that J3 involve in the PFT regulated heat stress response. In this study, the roles of J3 in protecting plants against prolong heat stress was also explored.
顯示於類別:	[生命科學研究所 ] 博碩士論文

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