|WANG, HONG - Jiangsu Academy Agricultural Sciences|
|LIN, JING - Jiangsu Academy Agricultural Sciences|
|CHANG, YOUHONG - Jiangsu Academy Agricultural Sciences|
Submitted to: Frontiers in Plant Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/31/2017
Publication Date: 2/15/2017
Citation: Wang, H., Lin, J., Chang, Y., Jiang, C. 2017. Comparative transcriptomic analysis reveals that Ethylene/H2O2-mediated hypersensitive response and program cell death determine the compatible interaction of Sand pear and Alternaria Alternata. Frontiers in Plant Science. 8:195. https://doi.org/10.3389/fpls.2017.00195.
Interpretive Summary: In plant-pathogen interactions, plant response to pathogens is based on two main mechanisms including microbe-associated molecular patterns (MAMPs) and the adaptive immune system. The action of plant resistance (R) genes belongs to the adaptive immune system. After recognition of pathogen, plant develops defense strategies against pathogen attack. These include the hypersensitive response (HR) and the programmed cell death (PCD) at the infection site, followed by the complicated defense response and metabolic changes in the surrounding tissues and distal un-infected parts. One of the earliest events in the HR is a burst of reactive oxygen species (ROS) including superoxide (O2-), hydroxyl radical (OH-) and subsequent accumulation of H2O2. The infection of an avirulent Pseudomonas syringae strain stimulated the production of O2- and H2O2, and induced defense-related gene expression and cell death in Arabidopsis. Whether ROS plays positive or negative roles during the HR is depending on the type of pathogens. For example, in Arabidopsis-P. syringae system, the accumulation of H2O2 induces cell death and restricts lesion development. However, in necrotrophic pathogen system, such as Botrytis cinerea and Sclerotinia sclerotiorum, pathogens proliferate on dead tissues caused by the generation of oxidative burst. Salicylic acid (SA), jasmonic acid (JA), ethylene (ET), as well as ROS, play key roles in PCD, as well as in the activation of plant defense responses. SA is required in plant resistance associated with the hypersensitive cell death during plant–pathogen interactions. At infection sites, SA binds to NON-EXPRESSOR OF PATHOGENESIS-RELATED GENES 3 (NPR3) and mediates degradation of the cell-death suppressor (NPR1), therefore, facilitating the occurrence of PCD and local effector-triggered immunity (ETI). NPR1 interacting with TGAs, bZIP transcription factors, directly promotes the expression of pathogenesis-related (PR) proteins such as PR1, BGL2 and PR5, and therefore limits growth of pathogen and contributes to resistance. Several studies suggest that SA-mediated signaling pathways are involved in resistance to biotrophic or hemibiotrophic pathogens. Pathogens also elicit JA and ET pathways. Unlike the SA pathway, a JA/ET-dependent defense provides strong resistance against necrotrophic pathogens that benefit from host cell death. JA and ET are considered to act synergistically in response to pathogens and activate defense-related gene expression in Arabidopsis. ETHYLENE RESPONSE FACTOR 1 (ERF1) integrates ET and JA signaling pathways to regulate the expression of downstream defense-related genes. Pathogen-induced expression of the plant defense-related genes such as Defensin (PDF1) or proteinase inhibitors I and II (PI I and PI II) is known as an indicator of the ET and JA responses. ET is also involved in the regulation of both the timing and degree of PCD during plant-pathogen interactions. An initiation of HR results in a large burst of ET. In addition, ET acts in concert with SA as a positive regulator of cell death progression in an Arabidopsis vad1 (vascular associated death 1) mutant. Transgenic petunia over-expressed A. thaliana ET receptor mutant ethylene-insensitive1-1 (etr1-1) inhibits senescence-associated genes PhCP8 and PhCP10 expression, thereby retards the senescence caused by B. cinerea infection. The role of ET-dependent pathway has been elucidated in AAL-toxin induced cell death. However, whether ET is involved in plant-Alternaria alternata (Fr) Keissler (AK-toxin) interactions is still largely unknown. Pears (Pyrus spp.) are one of the most important fruit trees in Europe, East Asia, and North America. Black spot disease, caused by the Japanese pear pathotype of Alternaria alternate (Fr.) Keisser, is one of the most serious diseases in Asia pear cultivation. Alternaria alternate (Fr.) Keisser produces h
Technical Abstract: A major production restriction on sand pear (Pyrus pyrifolia) is black spot disease caused by the necrotrophic fungus Alternaria alternata. However, pear response mechanism to A. alternata is unknown at molecular level. Here, host responses of a resistant cultivar Cuiguan (CG) and a susceptible cultivar Sucui1 (SC1) to A. alternata infection were investigated. We found that the primary necrotic lesion formed at 1 dpi and the expansion of lesions was aggressive in SC1. Data from transcriptomic profiles using RNA-Seq technology identified a large number of differentially expressed genes (DEGs) between CG and SC1 in the early phase of A. alternata infection. K-mean cluster and Mapman analysis revealed that genes involved in ethylene (ET) biosynthesis and ET signaling pathway such as ACS, ACOs, ERFs, and in hypersensitive response (HR) and programmed cell death (PCD) were significantly enriched and up-regulated in the susceptible cultivar SC1. Conversely, genes involved in response to hydrogen peroxide and superoxide were differentially up-regulated in the resistant cultivar CG after inoculation. Furthermore, ET levels were highly accumulated in SC1, but not in CG. Higher activities of detoxifying enzymes such as catalases were detected in CG. Our results demonstrate that the ET-/H2O2-mediated PCD and detoxifying processes play a vital role in the interaction of pear and A. alternata.