Signalling of Arabidopsis thaliana response to Pieris brassicae eggs shares similarities with PAMP-triggered immunity

Abstract

Insect egg deposition activates plant defence, but very little is known about signalling events that control this response. In Arabidopsis thaliana, oviposition by Pieris brassicae triggers salicylic acid (SA) accumulation and induces the expression of defence genes. This is similar to the recognition of pathogen-associated molecular patterns (PAMPs), which are involved in PAMP-triggered immunity (PTI). Here, the involvement of known signalling components of PTI in response to oviposition was studied. Treatment with P. brassicae egg extract caused a rapid induction of early PAMP-responsive genes. In addition, expression of the defence gene PR-1 required EDS1, SID2, and, partially, NPR1, thus implicating the SA pathway downstream of egg recognition. PR-1 expression was triggered by a non-polar fraction of egg extract and by an oxidative burst modulated through the antagonistic action of EDS1 and NUDT7, but which did not depend on the NADPH oxidases RBOHD and RBOHF. Searching for receptors of egg-derived elicitors, a receptor-like kinase mutant, lecRK-I.8, was identified which shows a much reduced induction of PR-1 in response to egg extract treatment. These results demonstrate the importance of the SA pathway in response to egg-derived elicitor(s) and unravel intriguing similarities between the detection of insect eggs and PTI in Arabidopsis.

Arabidopsis MYC Transcription Factors Are the Target of Hormonal Salicylic Acid/Jasmonic Acid Cross Talk in Response to Pieris brassicae Egg Extract

“…SA accumulates upon oviposition and the expression of SA-and NPR1-dependent genes (e.g. PR1) is activated (Little et al, 2007;Bruessow et al, 2010, Gouhier-Darimont et al, 2013. In addition, egg-induced SA accumulation is known to inhibit larvae-induced expression of JAdependent genes (e.g.…”

“…Expression of PATHOGENESIS-RELATED1 (PR1) is strongly up-regulated at the site of oviposition in response to P. brassicae eggs but also in response to egg extracts from other insect species, including the generalist Spodoptera littoralis (Bruessow et al, 2010). Findings that SA accumulates to high levels following P. brassicae oviposition and that mutants in ENHANCED DISEASE SUSCEPTIBILITY1, SALICYLIC ACID-DEFICIENT2 (SID2), and NPR1 are deficient in egg-induced PR1 expression indicate that eggs activate the SA pathway (Gouhier-Darimont et al, 2013;Bruessow et al, 2010). Interestingly, egg-induced SA was shown to antagonize the JA pathway by inhibiting the expression of insect-induced defense genes.…”

NAD Acts as an Integral Regulator of Multiple Defense Layers

“…4) and directly induces the expression of CHIT (Supplemental Fig. S12), a chitin-responsive gene (Gouhier-Darimont et al, 2013). Remarkably, an analysis of ROS burst in the cerk1-2 mutant impaired in the chitin response indicated reduced ROS production after NAD application (Supplemental Fig.…”

“…Briefly, four leaves from 5-week-old plants were pooled (n = 3), flash frozen in liquid nitrogen 20 h after infection with Pst-AvrRpm1 or 24 h after syringe infiltration with water or NAD + (1 mM), and then stored at 280°C until RNA extraction and RT-qPCR analyses. mRNA abundances were expressed relative to the ACTIN2 reference gene (At3g18780) using previously described gene-specific primers (Oelze et al, 2012;Pétriacq et al, 2012;Gouhier-Darimont et al, 2013;Gruner et al, 2013;Pétriacq et al, 2016). The sequences of RT-qPCR primers are given in Supplemental Table S4.…”

Spore Density Determines Infection Strategy by the Plant Pathogenic Fungus Plectosphaerella cucumerina

“…Four leaves from different plants were pooled (n = 4), flash frozen in liquid nitrogen at 2 and 5 dai, then stored at 280°C until RNA extraction, reverse transcriptase conversion, and quantitative PCR analyses, as described previously (Luna et al, 2014). PCR amplification of PR1 (At2g14610), PR5 (At1g75040), WKY70 (At3g56400), ICS1 (At1g74710), and VSP2 (At5g24770) was performed using previously described gene-specific primers (Gouhier-Darimont et al, 2013;Gruner et al, 2013;Li et al, 2013). Relative transcript quantities were calculated according to (1 + E)…”