Interactions of MAP Kinases, Histidine Kinase and YAP1 in the Citrus Fungal Pathogen Alternaria Alternate
Journal
植物病理學會刊
Journal Volume
23
Journal Issue
3&4
Start Page
293
End Page
301
ISSN
1021-9544
Date Issued
2014-09
Author(s)
Kuang-Ren Chung
Abstract
The tangerine pathotype of Alternaria alternata utilizes the AaFUS3, AaHOG1 and AaSLT2 MAP kinase-mediated signaling pathways, in conjunction with the two-component histidine kinase (AaHSK1) and the AaAP1 transcription regulator, for stress response, development and pathogenesis to citrus. This study reveals possible interactions among these pathways at transcriptional and post-translational levels. Systemic loss-of-function genetics in A. alternata revealed that both AaFUS3 and AaSLT2 are required for conidia formation. AaSLT2 mutant is hypersensitive to cell wall-degrading enzymes, yet AaHSK1 mutant is less sensitive and AaHOG1 mutant is highly resistant to them. Accumulation of the AaHOG1 gene transcript is up-regulated considerably in the AaSLT2 mutant and only slightly in the AaFUS3 mutant. AaSLT2 positively regulates AaFUS3 expression and vice versa. AaSLT2 also promotes AaAP1 expression, whereas AaAP1 inhibits AaSLT2 expression. Furthermore, phosphorylation of AaHOG1 or AaFUS3 protein is affected when other genes are inactivated, indicating a functional antagonism or synergism among these signal transduction pathways. Interestingly, signaling transduction pathways-mediated by AaAP1, AaHSK1, AaHOG1, AaSLT2, and AaFUS3 play a critical and non-redundant role for resistance to 2-chloro-5-hydroxypyridine or 2,3,5-triiodobenzoic acid, likely via regulation of common membrane transporters, in A. alternata.
柑橘鏈格孢病原真菌Alternaria alternata面臨逆境時、生長發育、或致病過程中，均需透過複雜的信號傳遞系統來調節細胞的生理生化的功能，以因應生長環境的變化。之前的研究已知信號傳遞系統，例如：絲裂原活化蛋白激酶（MAP kinases）, AaFUS3, AaHOG1 and AaSLT2，組氨酸激酶（histidine kinase, AaHSK1）及YAP1轉錄因子，在鏈格孢病原真菌中均扮演重要的角色。本研究進一步釐清這些信號傳遞系統之間的交互作用乃發生於轉錄或轉譯後的階層上。系統性的遺傳分析顯示鏈格孢病原真菌的AaFUS3及AaSLT2對分生孢子的產生能力極為重要。AaSLT2突變菌株對細胞壁分解酵素（CWDEs）非常敏感，AaHSK1突變菌株的感受性並未改變，但是AaHOG1突變菌株却對CWDEs有抗性。與野生型相較之下，AaHOG1基因的表達在AaSLT2突變菌株中大幅上升，但在AaFUS3突變菌株中增幅較不顯著。AaSLT2與AaFUS3基因的表達互相有正調控的關係。AaSLT2也能上調AaAP1的表達，相對地，AaAP1却抑制AaSLT2的表達。AaHOG1或AaFUS3蛋白磷酸化均受到AaHSK1、AaSLT2及AaAP1的調控。結果顯示這些信號傳遞分子之間在鏈格孢病原真菌細胞中有著相互拮抗或輔助的功能。有趣的是，上述每一個信號傳遞路逕對2-氯-5-羥基吡啶（2-chloro-5-hydroxypyridine）及2,3,5－三碘苯甲酸（2,3,5-triiodobenzoic acid）兩種藥劑的抗性均扮演重要角色。這些信號傳遞系統可能個别調控胞膜上的轉運蛋白，進而促使鏈格孢病原真菌細胞表現抗藥性。
Subjects
原生質體
virulence
oxidative stress
毒力
標的基因敲除
養逆境
major facilitator superfamily (MFS)
MFS運轉蛋白
protoplast
targeted gene disruption
Publisher
中華民國植物病理學會
Type
journal article