Overlapping Yet Response-Specific Transcriptome Alterations Characterize the Nature of Tobacco-Pseudomonas syringae Interactions.

Zoltán Bozsó,Ágnes Szatmári,Miklós Pogány,Evelin Kámán-Tóth,Péter G Ott,Gábor F Bognár

doi:10.3389/fpls.2016.00251

Abstract

In this study transcriptomic alterations of bacterially induced pattern triggered immunity (PTI) were compared with other types of tobacco–Pseudomonas interactions. In addition, using pharmacological agents we blocked some signal transduction pathways (Ca2+ influx, kinases, phospholipases, proteasomic protein degradation) to find out how they contribute to gene expression during PTI. PTI is the first defense response of plant cells to microbes, elicited by their widely conserved molecular patterns. Tobacco is an important model of Solanaceae to study resistance responses, including defense mechanisms against bacteria. In spite of these facts the transcription regulation of tobacco genes during different types of plant bacterial interactions is not well-described. In this paper we compared the tobacco transcriptomic alterations in microarray experiments induced by (i) PTI inducer Pseudomonas syringae pv. syringae type III secretion mutant (hrcC) at earlier (6 h post inoculation) and later (48 hpi) stages of defense, (ii) wild type P. syringae (6 hpi) that causes effector triggered immunity (ETI) and cell death (HR), and (iii) disease-causing P. syringae pv. tabaci (6 hpi). Among the different treatments the highest overlap was between the PTI and ETI at 6 hpi, however, there were groups of genes with specifically altered activity for either type of defenses. Instead of quantitative effects of the virulent P. tabaci on PTI-related genes it influenced transcription qualitatively and blocked the expression changes of a special set of genes including ones involved in signal transduction and transcription regulation. P. tabaci specifically activated or repressed other groups of genes seemingly not related to either PTI or ETI. Kinase and phospholipase A inhibitors had highest impacts on the PTI response and effects of these signal inhibitors on transcription greatly overlapped. Remarkable interactions of phospholipase C-related pathways with the proteasomal system were also observable. Genes specifically affected by virulent P. tabaci belonged to various previously identified signaling routes, suggesting that compatible pathogens may modulate diverse signaling pathways of PTI to overcome plant defense.

Highlights

Survival of plants is dependent on cellular recognition of microorganisms and a quick induction of defense responses
The P. syringae hrcC T3SS deficient mutant and the inactivated P. tabaci did not trigger any visible symptoms during the course of the experiments
Leaf materials were collected at 6 h after inoculations (6 hpi). This sampling time was chosen on the basis of our previous work since pattern triggered immunity (PTI) develops in tobacco by this time at 20◦C as detected by using various marker reactions (Burgyán and Klement, 1979; Ott et al, 1997, 2006; Bozsó et al, 1999, 2005; Klement et al, 1999, 2003; Szatmári et al, 2006, 2014)

Summary

Introduction

Survival of plants is dependent on cellular recognition of microorganisms and a quick induction of defense responses. Pathogenic, non-host pathogens, and saprophytic bacteria may enter the intercellular space of leaves passively e.g., via rain drops, or actively using their motile organelles on a leaf surface. The first layer of defense response activated in plant cells is triggered by microbe- or pathogen-associated molecular pattern(s) (MAMPs/PAMPs) of microorganisms (Mackey and McFall, 2006; Newman et al, 2013). MAMPs are common within groups of microbes (e.g., fungi or bacteria) irrespective of their life style i.e., pathogen or saprophytic. The MAMP-induced resistance response is called pattern triggered immunity (PTI), known as basal resistance. In compatible plant–pathogen interactions when bacteria are able to multiply the pathogen successfully blocks PTI (Jakobek et al, 1993; Hauck et al, 2003; Klement et al, 2003; Keshavarzi et al, 2004; Boller and He, 2009)

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