Journal of Integrative Plant Biology最新文献

Jasmonic acid (JA) is a critical signal controlling ripening and trait development in non-climacteric (NC) fruit. However, the mechanisms governing the JA biosynthesis remain unclear. Here, the signaling mechanisms for the JA biosynthesis are explored in strawberry (Fragaria vesca), a model NC fruit. The JA biosynthesis is demonstrated to be tightly coupled with the signaling of ABA, a pivotal signal controlling NC fruit ripening. When overexpressed or knocked out by CRISPR/Cas9 editing, FvSnRK2.6, a gene encoding a component of ABA signaling, promotes or inhibits JA production and aroma production, respectively. Moreover, FvSnRK2.6 phosphorylates FvJAZ12, a jasmonate ZIM-domain repressor, at the S142 residue, thereby promoting its degradation. Transforming the FvJAZ12 knockout mutant with FvJAZ12^S142A inhibits the production of ABA-induced aroma and JA. Furthermore, our current study reveals that FvMYC2, a transcription factor directly repressed by FvJAZ12, binds to cis-acting elements in the promoters of FvAOC3, FvAOS, FvLOX3, and FvOPR3, thus directly regulating JA biosynthesis. Thus, this study reveals an ABA signaling cascade that leads to JA biosynthesis, thereby elucidating the signaling mechanism governing the JA production during strawberry fruit ripening.

This commentary discusses new research showing that six structurally and functionally atypical NLR pairs in wheat confer disease resistance via a sensor NLR-helper NLR module. The functional mechanisms of some NLR pairs differ from the classical NLR pair model, revealing the complexity and diversity of the wheat immune system.

Plants and animals face the shared challenge of immune homeostasis. Tomato anti-systemin (antiSYS) and human interleukin-1 receptor antagonist (IL-1Ra) exemplify convergent strategies to restrain phytocytokine/cytokine signaling. Understanding this shared logic offers opportunities to fine-tune plant immunity, minimize growth trade-offs, and enhance crop resilience.

Soil salinization poses a global threat to agricultural productivity by degrading arable land. Preventing the rapid degradation of chlorophyll caused by saline-alkali stress is a crucial means to improve plant resistance and productivity. In this study, RNA sequencing identified CsPPH, a pheophytinase-encoding gene that functions as a negative regulator of both photosynthesis and saline-alkali tolerance in cucumber (Cucumis sativus L.). Saline-alkali stress rapidly induces the expression of related to APETALA2 2.12 (CsRAP2.12). Subsequently, CsRAP2.12 activates the transcription of both ethylene response factor 113-like (CsERF113L) and CsRAP2.7, while CsERF113L further transcriptionally regulates CsRAP2.7. CsERF113L promotes chlorophyll degradation and reactive oxygen species (ROS) accumulation both through direct transcriptional upregulation of CsPPH, chlorophyll b reductase (CsNYC1), and chlorophyllase 2 (CsCLH2) and by indirectly stimulating ethylene synthesis via upregulation of 1-aminocyclopropane-1-carboxylic acid synthase 6/9/10 (CsACS6/9/10), thereby impairing photosynthesis and accelerating senescence. CsRAP2.7 indirectly promotes saline-alkali stress-induced chlorophyll degradation and photosynthetic inhibition by facilitating CsERF113L-mediated transcriptional activation of CsPPH, CsCLH2, and CsACS6/9/10. Therefore, knockout of either CsRAP2.12, CsERF113L, or CsRAP2.7 significantly alleviated chlorophyll degradation and enhanced photosynthetic performance under saline-alkali stress, ultimately improving antioxidant capacity and stress tolerance. These findings reveal that the CsRAP2.12-CsERF113L/CsRAP2.7 module promotes saline-alkali stress-induced chlorophyll degradation and photosynthetic inhibition via a dual regulatory mechanism. Genetic disruption of this module significantly improves cucumber tolerance to saline-alkali stress.

This Commentary examines research by Wu et al. showing that β-1,3-glucan synthase-like 5 (GSL5) functions as a key gene for susceptibility to clubroot in Brassica family members by suppressing immunity regulated by jasmonic acid. Inaction of GSL5 through genome editing provides broad-spectrum resistance to clubroot.

Parent-of-origin effects are usually caused by selective expression of maternal or paternal alleles. Although genome-wide studies suggest that imprinted gene expression occurs primarily in the endosperm in plants, detailed studies of allele-specific gene expression and its associations with parent-of-origin phenotypes are scarce. NAC20 and NAC26 (NAC20/26 hereafter), a pair of tightly linked NAC-family transcription factors, redundantly regulate grain filling and albumin accumulation in rice endosperm. Here, we show that NAC20/26 exhibited allele-specific maternal expression, and the floury endosperm phenotype of the nac20/26 double mutant was inherited with a maternal effect. Further studies showed that the imprinted NAC20/26 expression and floury endosperm phenotype with a maternal effect are associated with insertions of two TEs in NAC20/26 of two Japonica rice varieties, but not in two Indica ones examined. The maternal NAC20/26 expression was associated with elevated DNA methylation in their paternal DMRs, and deletions of those TEs by gene editing led to decreased methylation in these DMRs, and biallelic NAC20/26 expression. Geographical analyses showed that Japonica varieties with high-latitude origins examined carried these TEs. These results establish that TE-mediated DNA methylation lead to grain filling with a maternal effect in high-latitude Japonica rice varieties, which may associate with northward expansion of rice during domestication.

A haplotype-resolved telomere-to-telomere genome reveals that the bird-shaped turquoise flowers of Strongylodon macrobotrys (jade vine) arise from co-pigmentation between the anthocyanin malvin and the flavonoid saponarin, shaped by genome dynamics and geological event-associated expansions of long terminal repeat retrotransposons.

The burgeoning multi-omics data have provided deep insights into the regulatory mechanisms underlying plant growth and development. However, revealing the complete landscape of gene regulatory networks underpinning various developmental processes remains challenging. Here, a multi-omics integrative gene network of the pear fruit development process was constructed through integrating 3D genomic, transcriptomic, transcription factor (TF) binding, chromatin accessibility, protein structure, and proteomic data. This integrative network comprises over 45,678 elements interconnected by more than 3.15 million edges and exhibits great potential in predicting regulatory and interactive relationships involved in the formation of key fruit quality traits (e.g., sugar, stone cell). In particular, the integrative network was applied to predict interactors of PbrII5, an inhibitor of vacuolar sucrose hydrolysis, and the predicted interactors were further validated through molecular experiments. Moreover, the network showed good performance in automatically predicting fruit trait-related genes by leveraging machine learning models. Specifically, a set of sugar metabolism-related genes was newly predicted, and their functions were verified through overexpression in pear fruit. In addition, extensive regulatory network divergence was observed between duplicated genes, with neofunctionalization being the dominant evolutionary process reshaping network connections of duplicated genes. Lastly, a multi-omics network database, pearGRN (http://peargrn.njau.edu.cn), was developed to facilitate further research for resolving complex gene regulatory relationships. This study lays a strong foundation for revealing novel regulatory mechanisms underlying fruit development and quality formation.

Argonaute proteins (AGOs) are central to RNA silencing pathways and play critical roles in plant antiviral defense. However, the functions of individual AGOs in rice remain incompletely understood. In this study, we demonstrate that rice AGO2 contributes to resistance against rice ragged stunt virus (RRSV) through a regulatory module involving miR167g-3p and its target gene, SNAP32. Immunoprecipitation coupled with small RNA sequencing revealed that AGO2 associates not only with virus-derived small interfering RNAs (vsiRNAs) but also preferentially associates with miR167g-3p during RRSV infection. Functional analyses further showed that miR167g-3p expression is induced upon infection. Transgenic rice lines overexpressing miR167g-3p exhibited enhanced resistance, whereas knockdown lines were more susceptible. SNAP32 was validated as a direct target of miR167g-3p through transient expression assays in Nicotiana benthamiana and dual-luciferase assays in rice protoplasts. Expression analyses confirmed that miR167g-3p represses SNAP32 at the transcript level. Consistently, SNAP32-overexpressing plants displayed increased susceptibility to RRSV, while snap32 knockout plants showed enhanced resistance, supporting a negative role of SNAP32 in antiviral defense. Together, these findings establish a regulatory pathway in which AGO2 promotes antiviral immunity by stabilizing miR167g-3p to repress SNAP32, thereby restricting RRSV infection. This work advances our understanding of AGO2-mediated defense in rice and highlights the use of a miRNA 3p strand within an AGO-miRNA-target module as an important layer of resistance against viral pathogens.

Somatic embryogenesis (SE) enables somatic cells to develop directly into embryos. SE is a major approach of regeneration, but recalcitrance to SE has become one of the main obstacles to biotechnology-aided breeding, especially for perennial woody plants. Citrus is one of the most important fruit crops in the world, and glycerol has long been used to induce SE from the embryogenic callus (EC) of citrus. Recently, we reported that CsIAA4-mediated repression of auxin signaling plays a critical role in glycerol-induced citrus SE, but the downstream signaling cascade remains to be elucidated. In this study, the HD-Zip transcription factor CsHAT14 was identified as a key downstream regulator of auxin signaling in citrus SE. CsARF5 directly promoted CsHAT14 expression, which repressed SE through suppression of critical regeneration-related genes (CsDOF3.4 and CsWOX13) and the auxin efflux gene CsPILS5. CsIAA4 interacted with CsARF5, and this interaction attenuated CsARF5-mediated transcriptional activation of CsHAT14, thereby de-repressed CsHAT14- directly suppressed genes including CsDOF3.4, and thus promoted SE. Knockdown of CsDOF3.4 resulted in downregulation of cell cycle-related genes and impaired SE. Our findings established the CsIAA4-CsARF5 and CsHAT14-CsDOF3.4 modules-mediated auxin signaling cascade that coordinates citrus SE, which advanced our understanding of the mechanisms underlying SE and supported improvement of regeneration efficiency in citrus biotechnology applications.