The role of Phanerochaete australis in enhancing defense activity against Magnaporthe oryzae in upland rice.

The inclusion of biological control in the integrated management of rice blast (Magnaporthe oryzae [Mo]) reduces pesticide application. Phanerochaete australis (Pha) has been shown to be a potential inducer of resistance to rice blast. Pha was isolated saprophytically from the rice phylloplane and studied for its interaction with Mo in the defense process of upland rice plants against the pathogen attack. Investigating the Pha × Mo interaction in a completely randomized design, the suppression of leaf blast and the epidemiological components of disease development were quantified in vivo, whereas the physiological and biochemical aspects, as defense enzymes and oxidative complex components, were evaluated in vitro during the induction of resistance. In the Pha × Mo interaction, it was found that seed treatment can significantly reduce disease severity by up to 93%, increase the photosynthetic apparatus, mobilize photoassimilates to the defense system, intensify defense enzyme and oxidant complex activities (chitinase [CHI], ß-1,3-glucanase [GLU], lipoxygenase [LOX], phenylalanine ammonia-lyase [PAL], poliphenoloxidase [PPO], peroxidase [POX], catalase [CAT], cuperoxide dismutase [SOD]), decrease phenolic compounds (TPCs), and increase photosynthetic pigment levels compared with the negative control (Mo). When treating the seed, we are referring to an induction process where there is no physical contact between the pathogens. The enzymes produced by the interaction between the microorganisms validate this process; thus, Pha acts as an inducer of resistance to upland rice plants challenged with Mo.

Herbivore-specific plant volatiles prime neighboring plants for nonspecific defense responses.

Plants produce species-specific herbivore-induced plant volatiles (HIPVs) after damage. We tested the hypothesis that herbivore-specific HIPVs prime neighboring plants to induce defenses specific to the priming herbivore. Since Manduca sexta (specialist) and Heliothis virescens (generalist) herbivory induced unique HIPV profiles in Nicotiana benthamiana, we used these HIPVs to prime receiver plants for defense responses to simulated herbivory (mechanical wounding and herbivore regurgitant application). Jasmonic acid (JA) accumulations and emitted volatile profiles were monitored as representative defense responses since JA is the major plant hormone involved in wound and defense signaling and HIPVs have been implicated as signals in tritrophic interactions. Herbivore species-specific HIPVs primed neighboring plants, which produced 2 to 4 times more volatiles and JA after simulated herbivory when compared to similarly treated constitutive volatile-exposed plants. However, HIPV-exposed plants accumulated similar amounts of volatiles and JA independent of the combination of priming or challenging herbivore. Furthermore, volatile profiles emitted by primed plants depended only on the challenging herbivore species but not on the species-specific HIPV profile of damaged emitter plants. This suggests that feeding by either herbivore species primed neighboring plants for increased HIPV emissions specific to the subsequently attacking herbivore and is probably controlled by JA.

Immune receptor genes and pericentromeric transposons as targets of common epigenetic regulatory elements.

Pattern recognition receptors (PRR) and nucleotide-binding leucine-rich repeat proteins (NLR) are major components of the plant immune system responsible for pathogen detection. To date, the transcriptional regulation of PRR/NLR genes is poorly understood. Some PRR/NLR genes are affected by epigenetic changes of neighboring transposable elements (TEs) (cis regulation). We analyzed whether these genes can also respond to changes in the epigenetic marks of distal pericentromeric TEs (trans regulation). We found that Arabidopsis tissues infected with Pseudomonas syringae pv. tomato (Pst) initially induced the expression of pericentromeric TEs, and then repressed it by RNA-directed DNA methylation (RdDM). The latter response was accompanied by the accumulation of small RNAs (sRNAs) mapping to the TEs. Curiously these sRNAs also mapped to distal PRR/NLR genes, which were controlled by RdDM but remained induced in the infected tissues. Then, we used non-infected mom1 (Morpheus' molecule 1) mutants that expressed pericentromeric TEs to test if they lose repression of PRR/NLR genes. mom1 plants activated several PRR/NLR genes that were unlinked to MOM1-targeted TEs, and showed enhanced resistance to Pst. Remarkably, the increased defenses of mom1 were abolished when MOM1/RdDM-mediated pericentromeric TEs silencing was re-established. Therefore, common sRNAs could control PRR/NLR genes and distal pericentromeric TEs and preferentially silence TEs when they are activated.