The plant's innate immune system detects potential biotic threats through recognition of microbe-associated molecular patterns (MAMPs) or danger-associated molecular patterns (DAMPs) by pattern recognition receptors (PRR). A central regulator of pattern-triggered immunity (PTI) is the BRI1-associated kinase 1 (BAK1), which undergoes complex formation with PRR upon ligand binding. Although viral patterns inducing PTI are well known from animal systems, nothing similar has been reported for plants. Rather, antiviral defense in plants is thought to be mediated by post-transcriptional gene silencing of viral RNA or through effector-triggered immunity, i.e., recognition of virus-specific effectors by resistance proteins. Nevertheless, infection by compatible viruses can also lead to the induction of defense gene expression, indicating that plants may also recognize viruses through PTI. Here, we show that PTI, or at least the presence of the regulator BAK1, is important for antiviral defense of Arabidopsis plants. Arabidopsis bak1 mutants show increased susceptibility to three different RNA viruses during compatible interactions. Furthermore, crude viral extracts but not purified virions induce several PTI marker responses in a BAK1-dependent manner. Overall, we conclude that BAK1-dependent PTI contributes to antiviral resistance in plants.

Rapid and complex immune responses are induced in plants upon pathogen recognition. One form of plant defense response is a programmed burst in transcription and translation of pathogenesis-related proteins, of which many rely on ER processing. Interestingly, several ER stress marker genes are up-regulated during early stages of immune responses, suggesting that enhanced ER capacity is needed for immunity. Eukaryotic cells respond to ER stress through conserved signaling networks initiated by specific ER stress sensors tethered to the ER membrane. Depending on the nature of ER stress the cell prioritizes either survival or initiates programmed cell death (PCD). At present two plant ER stress sensors, bZIP28 and IRE1, have been described. Both sensor proteins are involved in ER stress-induced signaling, but only IRE1 has been additionally linked to immunity. A second branch of immune responses relies on PCD. In mammals, ER stress sensors are involved in activation of PCD, but it is unclear if plant ER stress sensors play a role in PCD. Nevertheless, some ER resident proteins have been linked to pathogen-induced cell death in plants. In this review, we will discuss the current understanding of plant ER stress signaling and its cross-talk with immune signaling.

Virus-induced diseases cause severe damage to cultivated plants, resulting in crop losses. Certain plant-virus interactions allow disease recovery at later stages of infection and have the potential to reveal important molecular targets for achieving disease control. Although recovery is known to involve antiviral RNA silencing, the specific components of the many plant RNA silencing pathways required for recovery are not known. We found that Arabidopsis thaliana plants infected with oilseed rape mosaic virus (ORMV) undergo symptom recovery. The recovered leaves contain infectious, replicating virus, but exhibit a loss of viral suppressor of RNA silencing (VSR) protein activity. We demonstrate that recovery depends on the 21-22 nt siRNA-mediated post-transcriptional gene silencing (PTGS) pathway and on components of a transcriptional gene silencing (TGS) pathway that is known to facilitate non-cell-autonomous silencing signalling. Collectively, our observations indicate that recovery reflects the establishment of a tolerant state in infected tissues and occurs following robust delivery of antiviral secondary siRNAs from source to sink tissues, and establishment of a dosage able to block the VSR activity involved in the formation of disease symptoms.

Tobamoviruses encode a silencing suppressor that binds small RNA (sRNA) duplexes in vitro and supposedly in vivo to counteract antiviral silencing. Here, we used sRNA deep-sequencing combined with transcriptome profiling to determine the global impact of tobamovirus infection on Arabidopsis sRNAs and their mRNA targets. We found that infection of Arabidopsis plants with Oilseed rape mosaic tobamovirus causes a global size-specific enrichment of miRNAs, ta-siRNAs, and other phased siRNAs. The observed patterns of sRNA enrichment suggest that in addition to a role of the viral silencing suppressor, the stabilization of sRNAs might also occur through association with unknown host effector complexes induced upon infection. Indeed, sRNA enrichment concerns primarily 21-nucleotide RNAs with a 5′-terminal guanine. Interestingly, ORMV infection also leads to accumulation of novel miRNA-like sRNAs from miRNA precursors. Thus, in addition to canonical miRNAs and miRNA*s, miRNA precursors can encode additional sRNAs that may be functional under specific conditions like pathogen infection. Virus-induced sRNA enrichment does not correlate with defects in miRNA-dependent ta-siRNA biogenesis nor with global changes in the levels of mRNA and ta-siRNA targets suggesting that the enriched sRNAs may not be able to significantly contribute to the normal activity of pre-loaded RISC complexes. We conclude that tobamovirus infection induces the stabilization of a specific sRNA pool by yet unknown effector complexes. These complexes may sequester viral and host sRNAs to engage them in yet unknown mechanisms involved in plant:virus interactions.

In the absence of specialized mobile immune cells, plants utilize their localized programmed cell death and Systemic Acquired Resistance to defend themselves against pathogen attack. The contribution of a specific Arabidopsis gene to the overall plant immune response can be specifically and quantitatively assessed by assaying the pathogen growth within the infected tissue. For over three decades, the hemibiotrophic bacterium Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326) has been widely applied as the model pathogen to investigate the molecular mechanisms underlying the Arabidopsis immune response.

MicroRNAs (miRNAs) are short RNA chains (20-24 bp) which are emerging as important regulators of gene expression. miRNAs are encoded by specific genes, and in Arabidopsis, 190 genes have presently been identified. It has been shown that miR399 is essential for the phosphate starvation response, and recent studies have shown transcriptional changes in a number of additional miRNAs in response to a shortage of phosphate. In this study, global profiles of the miRNA in shoots of Arabidopsis plants grown on limited phosphate or full nutrient in combination with sucrose feed were analysed using the miRCURY LNA microRNA Array system. Furthermore, changes in miRNA transcript were compared between a mutant lacking the transcription factor phosphate starvation responses 1 (PHR1) and wild-type plants. The global analysis identified miRNAs belonging to nine families to respond to P deprivation, sucrose or PHR1. Among these, miR399d, miR827, miR866, miR391 and miR163 were most prominently induced upon P starvation, whereas miR169b/c was strongly induced in previously starved plants when provided with sufficient P and more so when combined with an addition of sucrose. This study shows that array analysis is in general agreement with data obtained by other high-throughput technologies. The array data were confirmed by real-time reverse transcriptase-polymerase chain reaction analyses of selected pri-miRNAs. Our data corroborate the implication that several miRNAs are involved in the P-starvation response and further identify miR866 and miR163 as new candidates of miRNAs associated with the regulation of the P-starvation response.

Our results suggest that dermal fibroblasts can be applied to facilitate the diagnostic analysis of dystroglycanopathy patients as well as to study the pathogenic mechanism of POMT mutations. Characterization of the POMT1 substrate protein alpha-dystroglycan and POMT in vitro mannosyltransferase activity shows that the severity of the clinical phenotype of the patients analyzed is inversely correlated with POMT activity.

The plant hormone salicylic acid (SA) plays an essential role in the regulation of diverse biological processes throughout the entire lifespan of the plant. Twenty-five years ago, SA first emerged as an endogenous signal capable of inducing plant defence responses both at the site of infection and in the systemic tissue of the plant. Since then, SA-mediated signalling pathways have been extensively characterized and dissected using genetic and biochemical approaches. Current research is largely focused on the identification of novel SA downstream signalling genes, in order to understand their precise contributions to the phytohormonal cross-talk and signalling network. This will subsequently help us to identify novel targets that are important for plant health, and contribute to advances in modern agriculture. In this chapter we highlight recent advances in the field of SA biosynthesis and the discovery of candidates for systemic mobile signals. We also discuss the molecular mechanisms underlying SA perception. In addition, we review the novel SA signalling components that expand the scope of SA functions beyond plant immunity to include plant growth and development, endoplasmic reticulum (ER) stress, DNA repair and homologous recombination. Finally, we shed light on the roles of SA in epigenetically controlled transgenerational immune memory that has long-term benefits for plants.