Molecular plant pathology最新文献

Safflower (Carthamus tinctorius), a versatile economic crop of the Asteraceae family used for both medicinal and oil purposes, is widely cultivated worldwide. During its growth period, particularly during the harvesting phase, safflower is susceptible to fungal infections, leading to reduced product quality and yield. Currently, there is a lack of research on candidate genes associated with safflower disease resistance, which hinders the breeding of disease-resistant varieties of safflower. The disease severity index of 499 safflower germplasm lines during the flowering period was analysed through genome-wide association studies (GWAS), and a highly correlated TLP (thaumatin-like proteins) family disease resistance candidate gene, CtTLP13, was identified. Subsequently, transcriptomic and proteomic analyses were conducted to characterise the molecular features of safflower under fungal infection, and it was confirmed that CtTLP13 can respond to the biotic stress when safflower is infected by Botrytis cinerea. CtTLP13 overexpression in Arabidopsis and safflower enhanced safflower disease resistance; in vitro experiments confirmed its inhibition of B. cinerea growth and spore germination. We isolated safflower extracellular vesicles (EVs), verified CtTLP13 localisation within them and showed that CtTLP13-carrying safflower EVs are taken up by B. cinerea and inhibit the fungal growth. Overall, this study identified a valuable disease resistance gene (CtTLP13) in safflower. We also investigated the role of safflower EVs in disease resistance, and the results showed that safflower EVs exhibit anti-B. cinerea activity.

Members of Fusarium sambucinum species complex (FSAMSC), major mycotoxigenic phytopathogens, affect cereal crops such as wheat and rice. The predominant members of FSAMSC, F. graminearum, F. asiaticum, and F. meridionale, are distinguished by their trichothecene chemotypes, primarily nivalenol (NIV) and deoxynivalenol (DON) chemotype. While DON has been linked to virulence in certain FSAMSC species, NIV chemotypes exhibit increased aggressive in rice, whereas DON chemotypes preferentially infect wheat. However, the genetic factors driving these chemotype-host associations remain unclear. This study investigated the genetic linkage between DON/NIV chemotype and host preference through molecular and phenotypic analyses. RNA sequencing revealed host-dependent differential expression of trichothecene biosynthetic (TRI) genes during wheat and rice infection by DON and NIV chemotypes. Sequencing confirmed that NIV chemotypes carry a functional TRI13 gene encoding a trichothecene C-4 hydroxylase, whereas DON chemotypes harbour a nonfunctional TRI13 pseudogene (ψTRI13). Genetic manipulation of TRI13 confirmed its role in determining DON/NIV chemotype and host preference. TRI13 deletion in NIV strains converted them into a DON chemotype, while complementation of ψTRI13 in DON strains generated a hybrid chemotype producing both toxins, with the 3-acetyl-DON chemotype showing a more pronounced hybrid profile than the 15-acetyl-DON chemotype. Pathogenicity assays revealed that TRI13 deletion reduced virulence in rice but enhanced colonisation in wheat. Conversely, TRI13 complementation increased rice aggressiveness and decreased wheat infection. This study provides the first genetic evidence for host preference driven by DON/NIV chemotypes in F. graminearum, F. asiaticum, and F. meridionale, offering insights for improved mycotoxin surveillance and disease management strategies.

Fhb1 is the most widely used locus for Fusarium head blight (FHB) resistance in wheat, yet the mechanistic basis of its candidate gene, TaHRC, remains elusive. Here, we demonstrate that the protein from the resistant allele TaHRC-R localises to both the nucleus and cytoplasm, whereas the susceptible protein TaHRC-S is confined to the nucleus. Remarkably, only TaHRC-R triggered a reactive oxygen species (ROS) burst in planta, dependent on its extranuclear localisation. The N-terminal 21 amino acids that distinguish TaHRC-R from TaHRC-S were essential for its nuclear export and ROS induction. Within the nucleus, TaHRC-R formed heterodimers with TaHRC-S via its N-terminal 21 amino acids and central region, disrupting the formation of large, sparse TaHRC-S condensates and converting them into numerous smaller assemblies. These results reveal a dual, spatially coordinated mechanism whereby TaHRC-R promotes ROS production outside the nucleus while modulating nuclear condensate dynamics to counteract the susceptible allele. This compartmentalised functionality provides a molecular framework for Fhb1-mediated resistance and illustrates a novel paradigm of subcellular specialisation in plant immunity.

Glycoside hydrolase family 17 (GH17) plays a critical role in degrading pathogen cell walls and is involved in plant defence responses against biotic stress. However, the functional roles of GH17 members in pepper in response to Phytophthora capsici, the causal agent of Phytophthora blight, remain unexplored. In this study, a total of 55 CaGH17 genes were identified in the pepper genome and classified into three distinct subfamilies based on phylogenetic relationships. Transcriptome analysis of both the resistant cultivar 17-p63 and the susceptible cultivar 16-217 inoculated with P. capsici at multiple time points revealed that CaGH17-12 exhibited markedly increased expression in the resistant cultivar, while no significant changes were observed in the susceptible cultivar at 60 h post-inoculation. Yeast secretion trap and subcellular localisation assays indicated that CaGH17-12 is secreted into the apoplast. The purified CaGH17-12 protein, expressed in yeast, exhibited β-glucan hydrolase activity, confirming its enzymatic function. Virus-induced gene silencing of CaGH17-12 significantly increased susceptibility to P. capsici, confirming its role in mediating Phytophthora blight resistance. CaGH17-12-silenced pepper plants exhibited reduced expression of jasmonic acid (JA)-related and reactive oxygen species (ROS)-associated genes. Moreover, exogenous application of β-glucan oligosaccharides, the putative hydrolytic products of CaGH17-12, induced pepper resistance to P. capsici by enhancing the production of ROS and activating the expression of defence-related genes. Taken together, these findings identified and characterised the CaGH17 gene family in pepper, highlighting the potential role of CaGH17-12 in conferring resistance to P. capsici through modulation of ROS accumulation and JA signalling.

Erwinia amylovora, the causative agent of fire blight, poses a threat to pome fruit production worldwide. Disease initiation involves a transition from an epiphytic to an endophytic growth stage, with early activation of the type III secretion system (T3SS) on floral stigmas enabling host tissue invasion. Among the diverse arsenals of E. amylovora, the T3SS and its effectors (T3Es), along with the exopolysaccharide amylovoran, represent core pathogenicity determinants. Systemic colonisation and persistence within the host are orchestrated by a complex regulatory network that coordinates transitions between motile planktonic and sessile biofilm-associated states. Central to this regulation are four conserved two-component systems (HrpX/HrpY, RcsC/RcsB, GrrS/GrrA and EnvZ/OmpR) and the second messenger cyclic-di-GMP (c-di-GMP). This review synthesises current knowledge across four interrelated themes: (i) the disease cycle and host colonisation strategies of E. amylovora and host defence response, (ii) pathogenicity and virulence factors of E. amylovora and their regulatory mechanisms, (iii) regulatory circuits modulating lifestyle transitions during systemic colonisation by the pathogen focusing on the role of c-di-GMP and two-component systems and (iv) evolutionary perspectives on the two-component systems and c-di-GMP along with comparisons to related enterobacterial pathogens. These insights advance our understanding of the molecular basis of fire blight pathogenesis and adaptative strategies employed by E. amylovora to thrive in diverse host environments.

Tung wilt disease, caused by Fusarium oxysporum f. sp. fordiis (Fof-1), poses a serious threat to tung oil tree (Vernicia fordii) production. Fortunately, another native Vernicia species in China, V. montana (woody tung oil tree) exhibits high resistance ability to the pathogen. The resistant and susceptible tung trees provide material for the investigation on the mechanism underlying the resistance to Fusarium wilt disease. Root xylem extracts of resistant V. montana significantly inhibited Fof-1 growth compared with that of susceptible V. fordii. Metabolomic analysis of V. montana root xylem revealed that 13 types of flavonoids increased after Fof-1 infection. Of the 13 flavonoids, antimicrobial assays showed that catechin, (-)-epicatechin and (-)-epigallocatechin exhibited an obvious inhibitory effect on Fof-1 growth. Transcriptomic analysis revealed that several genes with up-regulated expression patterns were also enriched in the flavonoid biosynthesis pathway after Fof-1 infection in V. montana. Among them, the anthocyanidin reductase (ANR) gene is directly involved in the biosynthesis of antimicrobial (-)-epicatechin and (-)-epigallocatechin. Moreover, transgenic V. montana lines overexpressing the VmANR gene elevated eight types of flavonoid concentrations, and silencing VmANR resulted in a substantial reduction in the levels of catechin and myricitrin. The enzyme activity assay in vitro further verified that VmANR catalysed the formation of (-)-epigallocatechin from the substrate cyanidin. This study identifies VmANR as a critical gene to promote biosynthesis of antimicrobial flavonoids in shaping resistance to Fof-1 infection, and offers an effective strategy for breeding Fusarium-resistant tung oil trees.

CaM-binding Protein 60-like G (CBP60g) and Systemic Acquired Resistance Deficient 1 (SARD1) are key immune signalling regulators that redundantly promote salicylic acid (SA) biosynthesis and plant immunity. Pathogen effectors often target these immune nodes to suppress plant defence. However, the role of bacterial effectors in disabling CBP60g and SARD1 to increase plant susceptibility remains unclear. In this study, we show that RipAW, an E3 ligase effector from Ralstonia solanacearum, induces root architecture changes and enhances plant susceptibility to R. solanacearum in Est::RipAW transgenic plants. The constitutively expressed RipAW (C177S), lacking E3 ligase activity, did not affect root architecture or plant susceptibility, indicating that RipAW's E3 ligase activity is crucial for these phenotypes. Transcriptional profiling of Est::RipAW plants revealed strong up-regulation of CBP60g and SARD1, while the SA signalling pathway remained in a basal state. Transient expression of RipAW and CBP60g in Nicotiana benthamiana showed that RipAW associates with CBP60g and affects its stability. Genetic analysis revealed that loss-of-function mutations in CBP60g and SARD1 increased plant susceptibility to R. solanacearum, but did not enhance RipAW-mediated pathogen growth. Furthermore, growth of the R. solanacearum ΔRipAW null mutant strain was reduced in wild-type plants but restored in cbp60g/sard1 mutant plants, confirming that the promotion of RipAW on bacterial growth is dependent on CBP60g and SARD1. Surprisingly, CBP60g and SARD1 were not involved in R. solanacearum-induced and RipAW-triggered root architecture changes. Overall, our findings demonstrate that RipAW increases plant susceptibility to R. solanacearum via both CBP60g/SARD1-dependent and -independent pathways.

MicroRNAs (miRNAs) are a class of noncoding RNAs that play important roles in regulating gene expression. They are involved in various biological processes, including plant growth, development, hormone signalling pathways and defence responses. Numerous studies have demonstrated the crucial role of miRNA in modulating plant immunity against various pathogens, including fungi, bacteria, viruses, nematodes and oomycetes. In this review, we synthesise recent advances in defence-related miRNAs in response to pathogens, highlighting their effects on plant-pathogen interactions and their functions in regulating hormone signalling pathways. Additionally, we explore the potential of small RNA-based technology tools in protecting plants from pathogens, including artificial microRNA, synthetic trans-acting small interfering RNA and RNA interference techniques, such as spray-induced gene silencing, host-induced gene silencing and virus-induced gene silencing.

Lipopolysaccharide (LPS) is a critical component of the bacterial outer membrane, which serves as a permeability barrier and site for sensing environmental signals. The structure and functional significance of LPS vary among bacterial species, influencing pathogenic traits. In this study, we aimed to investigate LPS biosynthesis genes in Pectobacterium carotovorum PCC27, the causal agent of bacterial soft rot in vegetable crops, and characterise the effects of their disruptions on virulence. Mutants lacking any LPS component exhibited reduced rotting symptoms on the midrib of kimchi cabbage and antimicrobial resistance, underscoring the importance of an intact LPS for virulence. The absence of O-antigen components did not affect the expression of major virulence factors; however, LPS core defects significantly impaired bacterial multiplication in planta, proteolytic activity and motility, which were progressively suppressed with greater truncations. Complementation analyses revealed that gene overexpression failed to restore these mutant phenotypes to the wild-type levels. Furthermore, western blot-based assembly assays of the type I secretion system demonstrated that LPS core truncation disrupted the outer membrane component PrtF localization. Additionally, the antiterminator factor RfaH was found to activate a large gene cluster directly involved in O-antigen biosynthesis, although it was dispensable for virulence. Together, these findings highlight the critical role of the LPS core in the functional assembly of outer membrane apparatuses, thereby contributing to virulence in P. carotovorum.