當環境溫度比正常所生長的溫度高出5-10度時，原核和真核生物都會對高溫產生反應而合成熱休克蛋白質。小分子量熱休克蛋白質的分子量約為15-30 kDa，是高等植物中含量最豐富的蛋白質，因此被視為高等植物體內所特有的一群蛋白質。從高山植物黃菀（senecio nemorensis）中找到葉綠體型熱休克蛋白質，利用葉綠體型熱休克蛋白質基因當成模式基因，瞭解小分子量熱休克蛋白質的調節機制。結果顯示除了熱逆境外，也有許多的逆境，如寒害及H2O2都會誘導這類熱休克蛋白質的表現，同時冬天在當地所採集的樣品中也可以偵測到此基因的表現。 另方面，為改善長時間的低溫處理誘導蝴蝶蘭開花時，對植物產生傷害的現象，利用農桿菌將低溫有關的基因，如大麥的HVA1基因、阿拉伯芥中與春化作用 有關的開花基因（At.FLC; At.VRN1）轉殖進入蝴蝶蘭中，以期能獲得低溫穩定調控的蝴蝶蘭品系，但經過長時間的轉殖實驗，並沒有成功的獲得到蝴蝶蘭轉植株。 Both eukaryotes and prokaryotes respond to high temperature by synthesizing heat shock proteins (HSPs) when environmental temperature were elevated 5℃ to 10℃ above normal growth temperature. Small HSPs (sHSPs) are ranging in size from 15 to 30 kDa. and represent the most abundant family of HSPs in higher plants. We have cloned chloroplast small heat shock proteins (CPsHSPs) from the high mountain plants, Senecio nemorensis. Using CPsHSPs as a model gene, we try to understanding of the regulatory mechanism of sHSPs. The results showed that many other stresses such as chilling, H2O2 can induce CPsHSPs expression. Interestingly, CPsHSPs was detected in the local samples which are growing in winter season. In order to alleviate the damage of Phalaenopsis plants when long term of chilling treatment, which is the condition for inducing flowering in Phalaenopsis, we try to transfer HVA1 (a LEAIII gene from barley), At.FLC, and At.VRN1 (flowering genes from Arabidopsis thaliana) genes into Phalaenopsis plants. The major aim is to control flowering time and alleviate the damage induced by low temperature in Phalaenopsis. However, no transgenic plants are established so far.
