鈣離子依賴磷酸激脢參與在植物先天性免疫反應以及荷爾蒙相關防禦反應之功能性分析

Abstract

在植物面對各式生物性或非生物逆境時、細胞內鈣離子累積為普遍且廣泛的訊息傳遞。在阿拉伯芥有一群包含34成員的鈣離子依賴蛋白磷酸激脢家族，同時具有磷酸激脢以及與鈣離子結合的能力，以此參與鈣離子訊息傳遞。其中鈣離子依賴蛋白磷酸激7與膜受體感受病原相關分子模式激活的免疫反應(PTI)正調控子LecRK VI.2可能有共表現之現象，對於典型PTI機制如MAPK磷酸化以及癒傷葡聚醣(callose)累積負調控。更多證據顯示，鈣離子依賴蛋白磷酸激7亦參與在荷爾蒙相關的、水楊酸防禦反應、茉莉酸-乙烯防禦反應，例如突變株對於活體營養性病原菌具有抗性但對於死體營養病原菌更感病，荷爾蒙標誌基因分析水楊酸途徑相對應的PR1有更高的表現，而茉莉酸-乙烯途徑標誌基因PDF1.2則相對低，顯示了此基因可能會影響兩個重要植物荷爾蒙平衡；另外，PEPR 抗病途徑亦於本基因的突變株當中亦顯示出了更佳之活性。綜合以上所述，在植物抗病反應當中，CPK7負向調控了PTI並且影響PEPR抗病途徑與荷爾蒙相關防禦反應。

Calcium ions (Ca2+) play an essential and general role as secondary messengers in many cellular signaling pathways. In Arabidopsis, Ca2+-dependent protein kinases (CPKs), a family of 34 members, are able to sense and to response to changes in calcium concentrations through their calcium binding ability and kinase activity. Among these CPKs, CPK7 was selected as a putative co-expressed gene with LecRK-VI.2, a positive regulator of PAMP-triggered Immunity (PTI). In this work, we show that CPK7 negatively regulates typical PTI responses such as callose deposition and MAPK kinase phosphorylation. Concomitantly, knock-out mutant lines of CPK7 were more resistant to the hemibiotrophic pathogen Pseudomonas syringae pv. tomato DC3000 (Pst DC3000). By contrast, cpk7 mutants were more susceptible to the necrotrophic pathogens Pectobacterium carotovorum ssp. carotovorum (Pcc) and Botrytis cinerea. The cpk7 mutants also demonstrated a potentiated accumulation of PR1 mRNA upon Pst DC3000 infection and less PDF1.2 up-regulation after Pcc inoculation, indicating that CPK7 may also affect hormone responses of plant defense. Furthermore, CPK7 also negatively regulates the (full name needed here) PEPR pathway. These results suggest that in response to calcium signaling triggered by PTI, CPK7 modulates hormone homeostasis and PEPR pathway activity, affecting plant defense to biotic stresses.