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Resistance (R) genes in the Triticeae tribe include not only genes encoding the canonical intracellular nucleotide-binding leucine-rich-repeat proteins (NLRs) but also genes encoding kinase fusion proteins (KFPs). Exploring these unconventional KFPs may expand the scope of effector-triggered immunity (ETI) and will have significant implications for crop improvement. [ABSTRACT FROM AUTHOR]

The regulation of stomatal aperture opening and closure represents an evolutionary battle between plants and pathogens, characterized by adaptive strategies that influence both plant resistance and pathogen virulence. The ongoing climate change introduces further complexity, affecting pathogen invasion and host immunity. This review delves into recent advances on our understanding of the mechanisms governing immunity-related stomatal movement and patterning with an emphasis on the regulation of stomatal opening and closure dynamics by pathogen patterns and host phytocytokines. In addition, the review explores how climate changes impact plant–pathogen interactions by modulating stomatal behavior. In light of the pressing challenges associated with food security and the unpredictable nature of climate changes, future research in this field, which includes the investigation of spatiotemporal regulation and engineering of stomatal immunity, emerges as a promising avenue for enhancing crop resilience and contributing to climate control strategies. Precise regulation of stomatal movement ensures plant resilience against pathogen infections and ever-fluctuating dynamics of the environment. This review navigates recent progress in revealing the intricate signaling mechanisms governing stomatal movement dynamics and patterning in plants upon pathogen infections under the shifting climate paradigms. [ABSTRACT FROM AUTHOR]

Bacterial pathogens deliver effectors into host cells mostly to manipulate signaling and metabolic molecules, thereby subverting host immunity. A recent study by Nomura et al. demonstrates that certain effectors create membrane channels in host cells, enabling bacteria to access water and solutes for multiplication. [ABSTRACT FROM AUTHOR]

Plant cell-wall perturbation upon environmental stress triggers adaptive cellular responses mediated by plasma membrane-resident sensors. We discuss a recent study by Bacete et al. showing that THESEUS1 (THE1) regulates plant cell adaptive responses to cell-wall disruption and update the working model for THE1 activation. [ABSTRACT FROM AUTHOR]

Plant elicitor peptide 1 (Pep1) is a versatile immune modulator that is involved in plant defense against herbivores and pathogens. A recent study (Hander et al. , Science , 2019) has uncovered that Arabidopsis thaliana Pep1 is released from the C-terminus of the tonoplast-resident precursor protein, PROPEP1, by Ca2+-activated metacaspases upon cell membrane rupture in damaged tissues. [ABSTRACT FROM AUTHOR]

Plant cell walls undergo dynamic structural and chemical changes during plant development and growth. Floral organ abscission and lateral root emergence are both accompanied by cell-wall remodeling, which involves the INFLORESCENCE DEFICIENT IN ABSCISSION ( IDA)-derived peptide and its receptors, HAESA ( HAE) and HAESA- LIKE2 ( HSL2). Plant cell walls also act as barriers against pathogenic invaders. Thus, the cell-wall remodeling during plant development could have an influence on plant resistance to phytopathogens. Here, we identified IDA-like 6 ( IDL6), a gene that is prominently expressed in Arabidopsis leaves. IDL6 expression in Arabidopsis leaves is significantly upregulated when the plant is suffering from attacks of the bacterial Pseudomonas syringae pv. tomato ( Pst) DC3000. IDL6 overexpression and knockdown lines respectively decrease and increase the Arabidopsis resistance to Pst DC3000, indicating that the gene promotes the Arabidopsis susceptibility to Pst DC3000. Moreover, IDL6 promotes the expression of a polygalacturonase ( PG) gene, ADPG2, and increases PG activity in Arabidopsis leaves, which in turn reduces leaf pectin content and leaf robustness. ADPG2 overexpression restrains Arabidopsis resistance to Pst DC3000, whereas ADPG2 loss-of-function mutants increase the resistance to the bacterium. Pst DC3000 infection elevates the ADPG2 expression partially through HAE and HSL2. Taken together, our results suggest that IDL6- HAE/ HSL2 facilitates the ingress of Pst DC3000 by promoting pectin degradation in Arabidopsis leaves, and Pst DC3000 might enhance its infection by manipulating the IDL6- HAE/ HSL2- ADPG2 signaling pathway. [ABSTRACT FROM AUTHOR]

Oidium heveae, an obligate biotrophic pathogen of rubber trees (Hevea brasiliensis), causes significant yield losses of rubber worldwide. However, the molecular mechanisms underlying the interplay between O. heveae and rubber trees remain largely unknown. In this study, we isolated an O. heveae strain, named HN1106, from cultivated H. brasiliensis in Hainan, China. We found that O. heveae HN1106 triggers the hypersensitive response in a manner that depends on the effector-triggered immunity proteins EDS1 (Enhanced Disease Susceptibility 1) and PAD4 (Phytoalexin Deficient 4) and on salicylic acid (SA) in the model plant Arabidopsis thaliana. However, SA-independent resistance also appears to limit O. heveae infection of Arabidopsis, because the pathogen does not produce conidiospores on npr1 (nonexpressor of pr1), sid2 (SA induction deficient 2) and NahG plants, which show disruptions in SA signalling. Furthermore, we found that the callose synthase PMR4 (Powdery Mildew Resistant 4) prevents O. heveae HN1106 penetration into leaves in the early stages of infection. To elucidate the potential mechanism of resistance of Arabidopsis to O. heveae HN1106, we inoculated 47 different Arabidopsis accessions with the pathogen, and analysed the plant disease symptoms and O. heveae HN1106 hyphal growth and conidiospore formation on the leaves. We found that the accession Lag2-2 showed significant susceptibility to O. heveae HN1106. Overall, this study provides a basis for future research aimed at combatting powdery mildew caused by O. heveae in rubber trees. [ABSTRACT FROM AUTHOR]

In plants, innate immune responses are initiated by plasma membrane-located pattern recognition receptors (PRRs) upon recognition of elicitors, including exogenous pathogen-associated molecular patterns (PAMPs) and endogenous damage-associated molecular patterns (DAMPs). Arabidopsis thaliana produces more than 1000 secreted peptide candidates, but it has yet to be established whether any of these act as elicitors. Here we identified an A. thaliana gene family encoding precursors of PAMP-induced secreted peptides (prePIPs) through an in-silico approach. The expression of some members of the family, including prePIP1 and prePIP2, is induced by a variety of pathogens and elicitors. Subcellular localization and proteolytic processing analyses demonstrated that the prePIP1 product is secreted into extracellular spaces where it is cleaved at the C-terminus. Overexpression of prePIP1 and prePIP2, or exogenous application of PIP1 and PIP2 synthetic peptides corresponding to the C-terminal conserved regions in prePIP1 and prePIP2, enhanced immune responses and pathogen resistance in A. thaliana. Genetic and biochemical analyses suggested that the receptor-like kinase 7 (RLK7) functions as a receptor of PIP1. Once perceived by RLK7, PIP1 initiates overlapping and distinct immune signaling responses together with the DAMP PEP1. PIP1 and PEP1 cooperate in amplifying the immune responses triggered by the PAMP flagellin. Collectively, these studies provide significant insights into immune modulation by Arabidopsis endogenous secreted peptides. [ABSTRACT FROM AUTHOR]

Plant pathogens usually promote pathogenesis by secreting effector proteins into host plant cells. One of the secreted effectors of P seudomonas syringae pv. phaseolicola, the causative agent of halo-blight disease in common bean ( P haseolus vulgaris), HopF1, activates effector-triggered immunity ( ETI) in a bean cultivar containing R1 resistance gene, but displays virulence function in a bean cultivar without the R1 gene. The virulence mechanism of the effector remained unknown, although it was identified more than a decade ago. Here we demonstrated that HopF1 can inhibit pathogen-associated molecular pattern-triggered immunity ( PTI) in a susceptible bean cultivar Tendergreen. HopF1 directly interacted with two RPM1-interacting protein 4 ( RIN4) orthologs of bean, PvRIN4a and PvRIN4b. Like RIN4 in A rabidopsis, both PvRIN4 orthologs negatively regulated the PTI responses in bean. However, the virulence function of HopF1 was enhanced in Tendergreen silencing PvRIN 4. Furthermore, silencing PvRIN 4a compromised the avrβ1-induced hypersensitive response ( HR), which previously was reported to be suppressed by HopF1. Together, these results demonstrated that PvRIN4 orthologs were not the virulence target of HopF1 for inhibiting PTI, but probably for interfering with ETI. [ABSTRACT FROM AUTHOR]

Oidium heveae HN1106, a powdery mildew (PM) that infects rubber trees, has been found to trigger disease resistance in Arabidopsis thaliana through ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1)‐, PHYTOALEXIN DEFICIENT 4 (PAD4)‐ and salicylic acid (SA)‐mediated signalling pathways. In this study, a typical TOLL‐INTERLEUKIN 1 RECEPTOR, NUCLEOTIDE‐BINDING, LEUCINE‐RICH REPEAT (TIR‐NB‐LRR)‐encoding gene, WHITE RUST RESISTANCE 4 (WRR4B), was identified to be required for the resistance against O. heveae in Arabidopsis. The expression of WRR4B was upregulated by O. heveae inoculation, and WRR4B positively regulated the expression of genes involved in SA biosynthesis, such as EDS1, PAD4, ICS1 (ISOCHORISMATE SYNTHASE 1), SARD1 (SYSTEMIC‐ACQUIRED RESISTANCE DEFICIENT 1) and CBP60g (CALMODULIN‐BINDING PROTEIN 60 G). Furthermore, WRR4B triggered self‐amplification, suggesting that WRR4B mediated plant resistance through taking part in the SA‐based positive feedback loop. In addition, WRR4B induced an EDS1‐dependent hypersensitive response in Nicotiana benthamiana and contributed to disease resistance against three other PM species: Podosphaera xanthii, Erysiphe quercicola and Erysiphe neolycopersici, indicating that WRR4B is a broad‐spectrum disease resistance gene against PMs. [ABSTRACT FROM AUTHOR]

A fluorescent pH-sensitive probe, 1-hydroxyl-3,4;9,10-tetra(n-butoxyloxycarbonyl)perylene (HPTBAC), was synthesized and used for pH sensing in living cells. The probe exhibits fluorescence emission characteristics with a pKa value of 7.9 and linear response to the very important pH range of 6.7–8.9. We designed a probe for binding the O− of hydroxyl in the perylene skeleton with H+ to possess the probing capability for detection in the acid to weak base pH range. The pH sensitivity is introduced via the O− moiety upon either protonation or deprotonation. In the deprotonation form, HPTBAC exhibits very weak emission due to strong electron-donating groups of O−. HPTBAC was successfully applied as a high-performance fluorochrome for living A549 cell (human lung cancer) and E. coli cell imaging. The results demonstrate that as a pH probe, HPTBAC is a good candidate for monitoring pH fluctuations in living cells. [ABSTRACT FROM AUTHOR]

Phytocytokines are plant peptide signals perceived by plasma membrane-localized receptors in regulating plant immunity. It was recently reported that the phytocytokine SERINE-RICH ENDOGENOUS PEPTIDE12 (SCOOP12) is recognized by the receptor kinase MALE DISCOVERER 1-INTERACTING RECEPTOR-LIKE KINASE 2 (MIK2) and activates plant immune responses and resistance to pathogens in Arabidopsis. Here, we show that Arabidopsis ENHANCER OF VASCULAR WILT RESISTANCE 1 (EWR1) and four EWR1 close propeptide homologs encode functional SCOOP peptides, which are able to activate immune responses via MIK2 and BRASSINOSTEROID INSENSITVE 1 (BRI1)-ASSOCIATED RECEPTOR KINASE 1 (BAK1) and SOMATIC EMBRYOGENESIS RECEPTOR KINASE 4 (SERK4). [ABSTRACT FROM AUTHOR]

The successful recognition of pathogen-associated molecular patterns (PAMPs) as a danger signal is crucial for plants to fend off numerous potential pathogenic microbes. The signal is relayed through mitogen-activated protein kinase (MPK) cascades to activate defenses. Here, we show that the Pseudomonas syringae type III effector HopF2 can interact with Arabidopsis thaliana MAP KINASE KINASE5 (MKK5) and likely other MKKs to inhibit MPKs and PAMP-triggered immunity. Inhibition of PAMP-induced MPK phosphorylation was observed when HopF2 was delivered naturally by the bacterial type III secretion system. In addition, HopF2 Arg-71 and Asp-175 residues that are required for the interaction with MKK5 are also necessary for blocking MAP kinase activation, PAMP-triggered defenses, and virulence function in plants. HopF2 can inactivate MKK5 and ADP-ribosylate the C terminus of MKK5 in vitro. Arg-313 of MKK5 is required for ADP-ribosylation by HopF2 and MKK5 function in the plant cell. Together, these results indicate that MKKs are important targets of HopF2. [ABSTRACT FROM AUTHOR]