Journal of Integrative Plant Biology最新文献

To adapt to environmental challenges, plants have evolved extensive gene families through duplication events, generating multiple-copy genes that mediate stress responses. However, the function of these duplicated genes in wheat remains unclear. In this study, we identified ten tandemly duplicated ETHYLENE RESPONSE FACTOR 109 (ERF109) genes in wheat, seven of which showed rapid induction under drought treatment. Overexpressing TaERF109A2 resulted in delayed heading date, increased tiller number, reduced plant height and root length, and enhanced drought resilience. Conversely, the CRISPR/Cas9-generated nonuple Taerf109s mutant showed exacerbated growth inhibition under drought stress. RNA-seq and functional analyses indicated that TaMADS56, functioning as a genetic downstream effector of TaERF109A2, modulates wheat tillering, heading date, and drought recovery responses. TaERF109A2 directly binds to the GCC-box motifs in the promoters of TaIPT8-5B/5D, thereby regulating cytokinin (CK) biosynthesis. Moreover, overexpression of TaERF109A2 enhances nicotianamine (NA) accumulation, which in turn confers tolerance to iron toxicity and drought stress via upregulation of nicotianamine synthase (NAS) genes. Our findings have highlighted the critical role of tandemly duplicated genes in the coordination of stress responses and developmental processes in wheat.

The circadian clock is an endogenous timekeeping mechanism that coordinates diverse biological processes across diverse organisms. Emerging evidence recently underscores its critical role in modulating plant immune responses. Salicylic acid (SA) is a central phytohormone in plant immunity; however, the molecular mechanisms by which clock components influence SA signaling under biotic stress are poorly understood. Here, we report the pivotal role of the core clock components, PSEUDO-RESPONSE REGULATOR 5 (PRR5) and PRR7, in governing Arabidopsis immunity by direct suppression of SA signaling. We found that the transcriptional outputs of SA signaling showed rhythmic expression and were remarkably affected by PRR5 and PRR7. Genetic analyses revealed that PRR5 and PRR7 function genetically upstream of the SA receptor NONEXPRESSER OF PATHOGENESIS-RELATED GENES 1 (NPR1) to inhibit SA-mediated defenses. Biochemical assays confirmed physical interactions among PRR5/7, NPR1, and TGA3, highlighting a direct mechanism whereby PRR5/7 antagonize the transcriptional activity of the NPR1-TGA3 complex. The prr5 prr7 double mutant not only showed enhanced SA signaling but also boosted pathogen-associated molecular pattern-triggered immunity, highlighting their broad inhibitory function in plant immunity. These findings provide critical insights into the temporal dynamics of plant immunity and reveal key molecular targets for breeding crop varieties with an optimized balance between growth and immunity.

Jasmonates (JAs) are vital to plant defense and stress adaptation. In Salvia miltiorrhiza, JA significantly promotes tanshinone accumulation, a class of bioactive diterpenoids. Although transcriptional regulation of JA signaling is well characterized, the post-translational mechanisms governing JA-mediated tanshinone biosynthesis remain poorly understood. Here, we identify SmWRKY2 as a critical regulator of JA-induced tanshinone accumulation, which interacts with SmCPK20. SmCPK20 positively regulates JA-induced tanshinone accumulation. JA signaling activates SmCPK20, promoting phosphorylation of SmWRKY2 at Thr-256. This phosphorylation event significantly enhances SmWRKY2's binding to the SmCPS1 promoter and its transcriptional activation capacity, thereby promoting tanshinone accumulation. Furthermore, SmWRKY2 interacts with the JA signaling repressor SmJAZ3. SmJAZ3 inhibits the SmWRKY2-SmCPK20 interaction in the absence of JA. JA-triggered degradation of SmJAZ3 releases SmWRKY2, enabling SmCPK20-mediated phosphorylation and promoting tanshinone biosynthesis. Collectively, our results demonstrate that JA and Ca²⁺ signaling pathways cooperate to regulate plant secondary metabolism.

Mitogen-activated protein kinase (MAPK) cascades regulate growth, development, stress responses, and immunity in plants by transmitting signals from upstream regulators to downstream components. In this study, we identify a MAPK cascade composed of MAPK kinase kinase 19 (MKKK19), three MAPK kinases (MKK3/MKK5/MKK9), and MAPK 6 (or MPK6) that is involved in Arabidopsis leaf senescence. The kinase oxidative signal-inducible 1 (OXI1) functions upstream of the MKKK19-MKK3/MKK5/MKK9-MPK6 cascade to promote leaf senescence, whereas two of RESPIRATORY BURST OXIDASE HOMOLOGS (RBOHs), RBOHD and RBOHF, act downstream to mediate the accumulation of reactive oxygen species (ROS). Loss-of-function mutation of OXI1, MKKK19, MKK3/MKK5/MKK9, or MPK6 resulted in delayed leaf senescence associated with reduced ROS levels, whereas transgenic lines overexpressing OXI1, MKKK19, MKK3/MKK5/MKK9, or MPK6 displayed the opposite phenotypes. Epistatic analyses supported the involvement of OXI1, MKKK19, MKK3/MKK5/MKK9, MPK6, and RBOHD/RBOHF in the same signaling pathway for leaf senescence. In conclusion, genetic and biochemical analysis of the Arabidopsis MKKK19-MKK3/MKK5/MKK9-MPK6 cascade through OXI1 and RBOHD/RBOHF revealed a vital role for the MAPK cascade and ROS in natural leaf senescence.

Plants are constantly challenged by diverse pathogens and respond through multilayered immune mechanisms described by the classical "zig-zag" model. Apoplast nanoparticles (ANs), extracellular vesicle (EV)-like entities, are dynamically remodeled during plant-pathogen interactions. Although EVs are known to carry immune-regulatory cargos, the specificity and coordination of ANs protein responses to distinct pathogens remain largely unresolved. Here, we show that the glycosylation profiles of ANs and their N-glycoproteins undergo distinct remodeling upon infection with Pseudomonas syringae and Botrytis cinerea, as revealed by lectin microarray and mass spectrometry analyses. We identify SPILR, an ANs protein that modulates bacterial morphology and motility by reducing polygalacturonase activity and inhibiting the bacterial flagellar P-ring protein, FlgI. Additionally, the ESM1 protein enhances Arabidopsis resistance to B. cinerea through modulation of lipase activity and lipid metabolism. Disruption of N-glycosylation sites on ANs proteins compromises their antimicrobial function and alters host resistance to both bacterial and fungal pathogens. Together, our findings uncover N-glycosylation as a critical determinant of ANs-mediated extracellular immunity, highlighting glycosylation as an integrative mechanism linking vesicle biology, pathogen specificity, and immune signaling. This work establishes a framework for glycoengineering-based strategies to enhance crop resistance and advance nano-agricultural applications.

Long non-coding RNAs (lncRNAs) play an important role in regulating plant growth and development, and stress response. However, their roles in Botrytis cinerea resistance remain poorly characterized. As a devastating necrotrophic fungus, gray mold is one of the most serious diseases that affects crop production worldwide. In this study, through screening of B. cinerea resistance in 18 strawberry germplasms, we identified Fragaria nilgerrensis as a resistant species and Fragaria nubicola as a susceptible one. We conducted lncRNA-seq on resistant and susceptible strawberries at 4 d after B. cinerea inoculation and untreated controls. lincRNA6679 and its target gene FnWRKY14 were identified in F. nilgerrensis. Coding potential assessment and RNA pull-down experiments revealed that lincRNA6679 is a long non-coding RNA that positively regulates FnWRKY14 expression by forming molecular complexes with FnWRKY50 or FnMYB59. Genetic transformation demonstrated that both lincRNA6679 and FnWRKY14 enhance resistance to B. cinerea in strawberries. Moreover, FnWRKY14 is bound to the FnPR1B promoter, activating its expression. FnWRKY14 was phosphorylated and activated by FnMAPK3 or FnMAPK6, further upregulating the expression of FnPR1B and enhancing disease resistance. This study revealed how long non-coding RNAs regulate strawberry resistance to B. cinerea, broadening the scope of research on strawberry resistance mechanisms and providing new strategies for molecular breeding.