Bacterial blight (BB) of rice caused by the phytopathogenic bacterium Xanthomonas oryzae pv. oryzae (Xoo) is a disease of global importance.  Xoo utilizes the type III secretion system (T3SS) and its effectors for virulence, and XopM is a conserved T3SS effector in Xanthomonas spp.  However, the virulence function of XopM is largely unknown.  In this study, we show that XopM contributes to Xoo virulence in rice.  We demonstrate that XopM interacts with allene oxide synthase OsAOS3, a key enzyme involved in jasmonic acid (JA) biosynthesis.  The expression levels of OsAOS3 and three homologues of OsAOS were elevated after Xoo infection.  Knockout mutants of OsAOS3 exhibited decreased JA accumulation and reduced resistance to Xoo and X. oryzae pv. oryzicola.  Moreover, JA-related defense genes were downregulated in osaos3 mutants during Xoo infection.  Based on our results, we propose a model showing how XopM hijacks OsAOS3 to interfere with JA-mediated defenses, leading to a suppression of rice immunity.  Our findings reveal a novel virulence strategy where Xanthomonas pathogens interfere with the JA pathway and modulate the host defense response.

Flavonols possess significant medical value and are essential for plant stress resistance.  These compounds constitute primary components of the nutritional value in onions, particularly in edible portions.  While the flavonol biosynthetic pathway has been extensively studied, its regulatory mechanisms in onions remain incompletely understood.  This investigation identified flavonol biosynthesis and regulatory genes through analysis of transcriptome and metabolomics data from different developmental stages of ‘SA1’.  Two R2R3-MYB transcription factors, AcMYB12 and AcMYB29, were identified as positive regulators of onion flavonol biosynthesis.  Transcriptional activation assays demonstrated that both could activate AcCHS, AcF3´H, and AcFLS.  Yeast one-hybrid assays confirmed their direct binding to these gene promoters.  The expression levels of flavonol pathway genes and flavonol contents in AcMYB12/AcMYB29-overexpressing onion calli and Arabidopsis plants were significantly higher than those in the control group.  Transient silencing assays revealed partial functional redundancy between these two transcription factors.  Notably, their regulatory capabilities exhibited significant differences.  AcMYB12 predominantly regulates flavonol accumulation, while AcMYB29 specifically influences quercetin.  Further investigation of the molecular mechanisms underlying differential regulation indicated variations in cis-elements within flavonol pathway gene promoters and differences in binding activity between transcription factors and cis-elements.

Ogura cytoplasmic male sterility (Ogura CMS) was first identified in wild radish (Raphanus sativus) and resulted in complete pollen abortion.  However, the molecular mechanism of Ogura CMS in Chinese cabbage remains unclear.  A cytological analysis confirmed nuclear degradation during the late uninucleate stage of pollen development, which diminished by the tricellular stage.  Concurrently, tapetal cells exhibited abnormal enlargement and vacuolation starting from the tetrad stage.  Serious developmental defects were observed in the pollen wall.  During early pollen development, genes associated with cytochrome c and programmed cell death (PCD) were upregulated in the Ogura CMS line, while genes involved in pollen wall mitosis were downregulated.  Conversely, at the late stage of pollen development, peroxisome and autophagy-related genes in the Ogura CMS line were upregulated.  The mitochondrial orf138 gene mutation triggered the PCD process in tapetal cells, leading to their abnormal enlargement and the degradation of their contents, eventually resulting in vacuolation at the tricellular stage.  These tapetal defects hindered the provision of adequate sporopollenin and nutrients to the microspores, consequently leading to abnormal pollen wall development and abnormal mitosis in the microspores.  Ultimately, nuclear dispersion commenced during the late uninucleate stage, and autophagy occurred in the late stage of pollen development.  Consequently, the plant could not produce functional pollen, resulting in male sterility in Chinese cabbage.  Studies of Ogura CMS can promote the production and application of male sterile materials and enrich male sterile resources, which is of great significance for hybrid breeding.

The velvet protein family serves as a crucial factor in coordinating development and secondary metabolism in numerous pathogenic fungi.  However, no previous research has examined the function of the velvet protein family in Fusarium oxysporum f. sp. niveum (FON), a pathogen causing a highly destructive disease in watermelon.  In this study, ∆fovel1 and ∆folae1 deletion mutants and ∆fovel1-C and ∆folae1-C corresponding complementation mutants of FON were validated.  Additionally, the phenotypic, biochemical, and virulence effects of the deletion mutants were investigated.  Compared to the wild-type strains, the ∆fovel1 and ∆folae1 mutants exhibited altered mycelial phenotype, reduced conidiation, and decreased production of bikaverin and fusaric acid.  Furthermore, their virulence on watermelon plant roots significantly decreased.  All these alterations in mutants were restored in corresponding complementation strains.  Notably, yeast two-hybrid results demonstrated an interaction between FoVel1 and FoLae1.  This study reveals that FoVEL1 and FoLAE1 play essential roles in secondary metabolism, conidiation, and virulence in FON.  These findings enhance our understanding of the genetic and functional roles of VEL1 and LAE1 in pathogenic fungi.