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Abstract
The plant immune system is divided into two branches; one branch is based on the recognition of pathogen-associated molecular patterns (PAMP-triggered immunity), and the other relies on pathogenic effector detection (effector-triggered immunity). Despite each branch being involved in different complex mechanisms, both lead to transcription reprogramming and, thus, changes in plant metabolism. To study the defense mechanisms involved in the Brassica oleracea–Xanthomonas campestris pv. campestris (Xcc) interaction, we analyzed the plant transcriptome dynamics at 3 and 12 days postinoculation (dpi) by using massive analysis of 3′-cDNA ends. We identified more induced than repressed transcripts at both 3 and 12 dpi, although the response was greater at 12 dpi. Changes in the expression of genes related to the early infection stages were only detected at 12 dpi, suggesting that the timing of triggered defenses is crucial to plant survival. qPCR analyses in susceptible and resistant plants allowed us to highlight the potential role of two calcium-signaling proteins, CBP60g and SARD1, in the resistance against Xcc. This role was subsequently confirmed using Arabidopsis knockout mutants.
Highlights
Plant leaves are relatively isolated from the environment by physical barriers that prevent desiccation and the penetration of phytopathogens
With the aim of deciphering the molecular mechanisms involved in the response to bacterial pathogenesis, we investigated the transcriptome dynamics of Brassica oleracea in response to Xanthomonas campestris pv. campestris (Xcc) race 1 infection at 3 and 12 days after inoculation
The major group corresponded to transcripts involved in phytohormone metabolism, which included important genes in the synthesis (lipoxygenases (LOX) or allele oxide synthase (AOS)) and perception (JAZ-proteins) of jasmonic acid (JA) and two methyl-transferases involved in the synthesis of methyl salicylate, an active form of salicylic acid (SA)
Summary
Plant leaves are relatively isolated from the environment by physical barriers (i.e., the cuticle) that prevent desiccation and the penetration of phytopathogens. Compatible pathogens can overcome this first barrier of the immune system and trigger a second level of defense called ETI (effectortriggered immunity), mediated by NB-LRR proteins, which occurs mainly intracellularly[2,4]. The burst of these mechanisms of defense has been associated with the activation of HR (hypersensitive response) and SAR (systemic acquired resistance)[5]. Pombo et al.[9] reported that as little as 14% of the Tortosa et al Horticulture Research (2019)6:103 transcriptomic changes occur in response to the attack of Pseudomonas syringae on tomato plants are common between PTI and ETI responses This apparent contradiction could be explained by the use of different plantpathogen systems. Tsuda and Katagari[3] reviewed the plant mechanisms in the response to different bacterial PAMPs and effectors, concluding that different PAMPs trigger the PTI response through common signaling pathways, whereas the cellular response to different pathogen effectors diverges among microbial types
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