乙烯是種化學結構簡單的氣體荷爾蒙，在植物的生活史中，從種子萌發，開花受粉，果實成熟，到植物老化，乙烯都扮演重要的角色。乙烯也會和植物體內的其他賀爾蒙 (例如水揚酸，茉莉酸及離層酸) 產生交互作用，讓植物能夠在逆境時產生適當的反應來適應環境的變化而求得生存。乙烯的生合成是SAM (S-adenosylmethionine)經過ACC (1-aminocyclopropane-1-carboxylic acid) 合成酶(ACS) 的催化形成ACC，再經由ACC氧化酶作用而產生。之前研究顯示，在阿拉伯芥中的ETO1 (ETHYLENE OVERPRODUCER1) 產生突變，會造成乙烯大量產生。因此可推論ETO1會負向調控乙烯的生合成。 ETO1屬於一個植物基因家族，包括EOL1及EOL2 (ETO1-LIKE) 共三個成員，帶有BTB (Broad-Complex, Tramtrack, and Bric a brac) 和 TPR (Tetratricopeptide Repeat) 的功能性區域。這兩個區域與蛋白質交互作用有關。本論文的研究是利用基因功能活化法 (activation tagging) 篩選及鑑定eto1-5突變株的抑制基因 (suppressor gene)；藉由篩選基因功能活化法所得到的突變株，找到16個seat (suppressor of eto1-5 by activation tagging) 的突變株，可有效抑制eto1-5性狀 (phenotype)，經由初步之生理及遺傳研究，確定所有seat突變株皆為顯性突變 (dominant mutation)。此外也鑑定這些突變株的T-DNA嵌入點 (insertion site) ，用以分析哪些鄰近基因可能是造成seat表現型態的原因。未來，將製備轉殖基因植物來證實所選擇的基因是否真的會抑制eto1-5的突變性狀。 Ethylene is a gaseous phytohormone and has a versatile role in plant physiology. Ethylene biosynthesis is committed by the conversion of S-adenosylmethionine (SAM) to 1-aminocyclopropane-1-carboxylic acid (ACC) by ACC synthase (ACS). Previous studies showed that ETO1 (ETHYLENE OVERPRODUCER1) negatively regulated ethylene biosynthesis and resulted in increased ethylene production in Arabidopsis thaliana. ETO1 represents a gene family in Arabidopsis thaliana, including EOL1 and EOL2 (ETO1-LIKE). There are two distinct protein domain in ETO1. BTB (Broad-Complex, Tramtrack, and Bric a brac) and TPR (Tetratricopeptide Repeat) domains, which both are involved in related with protein-protein interactions. My thesis research is to use activation T-DNA tagging approach to identify suppressors of eto1-5 in Arabidopsis thaliana. By screening the activation tagging mutants carrying an eto1-5 allele, we have found 16 seat (suppressor of eto1-5 by activation tagging) mutant lines. All of the 16 seat mutants are dominant and belong to at least 3 complementation groups. I have identified the T-DNA insertion sites in the seat mutants to analyse how the flanking genes regulate seedling phenotype of eto1-5. In the future work, Arabidopsis transgenic lines will be generated to confirm the function of selected genes as suppressors of eto1-5.
