Plant-pathogen interactions are known to be affected by environmental factors including temperature; however, the temperature effects have not been systematically studied in plant disease resistance. Here, we characterized the effects of a moderate increase in temperature on resistance to bacterial pathogen Pseudomonas syringae and two viral elicitors in Arabidopsis thaliana and Nicotiana benthamiana. Both the basal and the resistance (R) gene–mediated defense responses to Pseudomonas syringae are found to be inhibited by a moderately high temperature, and hypersensitive responses induced by R genes against two viruses are also reduced by an increase of temperature. These indicate that temperature modulation of defense responses to biotrophic and hemibiotrophic pathogens might be a general phenomenon. We further investigated the roles of two small signaling molecules, salicylic acid and jasmonic acid, as well as two defense regulators, EDS1 and PAD4, in this temperature modulation. These components, though modulated by temperature or involved in temperature regulation or both, are not themselves determinants of temperature sensitivity in the defense responses analyzed. The inhibition of plant defense response by a moderately high temperature may thus be mediated by other defense signaling components or a combination of multiple factors.

Plants and animals detect the presence of potential pathogens through the perception of conserved microbial patterns by cell surface receptors. Certain solanaceous plants, including tomato, potato and pepper, detect flgII-28, a region of bacterial flagellin that is distinct from that perceived by the well-characterized FLAGELLIN-SENSING 2 receptor. Here we identify and characterize the receptor responsible for this recognition in tomato, called FLAGELLIN-SENSING 3. This receptor binds flgII-28 and enhances immune responses leading to a reduction in bacterial colonization of leaf tissues. Further characterization of FLS3 and its signalling pathway could provide new insights into the plant immune system and transfer of the receptor to other crop plants offers the potential of enhancing resistance to bacterial pathogens that have evolved to evade FLS2-mediated immunity.

Summary: Disease resistance (R) proteins, as central regulators of plant immunity, are tightly regulated for effective defense responses and to prevent constitutive defense activation under non‐pathogenic conditions. Here we report the identification of an F‐box protein CPR1/CPR30 as a negative regulator of an R protein SNC1 likely through SCF (Skp1‐cullin‐F‐box) mediated protein degradation. The cpr1‐2 (cpr30‐1) loss‐of‐function mutant has constitutive defense responses, and it interacts synergistically with a gain‐of function mutant snc1‐1 and a bon1‐1 mutant where SNC1 is upregulated. The loss of SNC1 function suppresses the mutant phenotypes of cpr1‐2 and cpr1‐2 bon1‐1, while overexpression of CPR1 rescues mutant phenotypes of both bon1‐1 and snc1‐1. Furthermore, the amount of SNC1 protein is upregulated in the cpr1‐2 mutant and down‐regulated when CPR1 is overexpressed. The regulation of SNC1 by CPR1 is dependent on the 26S proteosome as a protease inhibitor MG132 stabilizes SNC1 and reverses the effect of CPR1 on SNC1. Interestingly, CPR1 is induced after infection of both virulent and avirulent pathogens similarly to the other negative defense regulator BON1. Thus, this study reveals a new mechanism in R protein regulation likely through protein degradation and suggests negative regulation as a critical component in fine control of plant immunity.

Ethylene (ET) signal transduction may regulate plant growth and defense, depending on which components are recruited into the pathway in response to different stimuli. We report here that the ET pathway controls both insect resistance (IR) and plant growth enhancement (PGE) in Arabidopsis (Arabidopsis thaliana) plants responding to harpin, a protein produced by a plant pathogenic bacterium. PGE may result from spraying plant tops with harpin or by soaking seeds in harpin solution; the latter especially enhances root growth. Plants treated similarly develop resistance to the green peach aphid (Myzus persicae). The salicylic acid pathway, although activated by harpin, does not lead to PGE and IR. By contrast, PGE and IR are induced in both wild-type plants and genotypes that have defects in salicylic acid signaling. In response to harpin, levels of jasmonic acid (JA) decrease, and the COI1 gene, which is indispensable for JA signal transduction, is not expressed in wild-type plants. However, PGE and IR are stimulated in the JA-resistant mutant jar1-1. In the wild type, PGE and IR develop coincidently with increases in ET levels and the expression of several genes essential for ET signaling. The ET receptor gene ETR1 is required because both phenotypes are arrested in the etr1-1 mutant. Consistently, inhibition of ET perception nullifies the induction of both PGE and IR. The signal transducer EIN2 is required for IR, and EIN5 is required for PGE because IR and PGE are impaired correspondingly in the ein2-1 and ein5-1 mutants. Therefore, harpin activates ET signaling while conscribing EIN2 and EIN5 to confer IR and PGE, respectively.

Harpin_Xoo, encoded by the hpaG_Xoo gene of Xanthomonas oryzae pv. oryzae, is a member of the harpin group of proteins that induce pathogen resistance and hypersensitive cell death (HCD) in plants. We elaborated whether both processes are correlated in hpaG_Xoo-expressing tobacco (HARTOB) plants, which produced harpin_Xoo intracellularly. Resistance to fungal, bacterial, and viral pathogens increased in HARTOB, in correlation with the expression of hpaG_Xoo, the gene NPR1 that regulates several resistance pathways, and defense genes GST1, Chia5, PR-1a, and PR-1b that are mediated by different signals. However, reactive oxygen intermediate burst, the expression of HCD marker genes hsr203 and hin1, and cell death did not occur spontaneously in HARTOB, though they did in untransformed and HARTOB plants treated exogenously with harpin_Xoo. Thus, the transgenic expression of harpin_Xoo confers nonspecific pathogen defense in the absence of HCD.