Plants can be infected by a variety of pathogens, most of which can cause severe economic losses. The plants resist the invasion of pathogens via the innate or acquired immune system for surviving biotic stress. The associations between plants and pathogens are sophisticated beyond imaging and the interactions between them can occur at a very early stage after their touching each other. A number of researchers in the past decade have shown that many biochemical events appeared even as early as 5 min after their touching for plant disease resistance response. The early molecular interactions of plants and pathogens are likely to involve protein phosphorylation, ion fluxes, reactive oxygen species (ROS) and other signalling transduction. Here, we reviewed the recent progress in the study for molecular interaction response of fungal pathogens and host plant at the early infection stage, which included many economically important crop fungal pathogens such as cereal rust fungi, tomato Cladosporium fulvum , rice blast and so on. By dissecting the earlier infection stage of the diseases, the avirulent/virulent genes of pathogen or resistance genes of plant could be defined more clearly and accurately, which would undoubtedly facilitate fungal pathogenesis study and resistant crop breeding.

Molecular and genomic studies have shown the presence of a large number of SPX gene family members in plants, some of which have been proved to act in P signalling and homeostasis. In this study, the molecular and evolutionary characteristics of the SPX gene family in plants were comprehensively analysed, and the mechanisms underlying the function of SPX genes in P signalling and homeostasis in the model plant species Arabidopsis ( Arabidopsis thaliana ) and rice ( Oryza sativa ), and in important crops, including wheat ( Triticum aestivum ), soya beans ( Glycine max ) and rapeseed ( Brassica napus ), were described. Emerging findings on the involvement of SPX genes in other important processes (i.e. disease resistance, iron deficiency response, low oxygen response and phytochrome-mediated light signalling) were also highlighted. The available data suggest that SPX genes are important regulators in the P signalling network, and may be valuable targets for enhancing crop tolerance to low P stress. Further studies on SPX proteins should include more diverse members, which may reveal SPX proteins as important regulatory hubs for multiple processes including P signalling and homeostasis in plants.

Summary: Root hair development is crucial for phosphate absorption, but how phosphorus deficiency affects root hair initiation and elongation remains unclear. We demonstrated the roles of auxin efflux carrier PIN‐FORMED2 (PIN2) and phospholipase D (PLD)‐derived phosphatidic acid (PA), a key signaling molecule, in promoting root hair development in Arabidopsis thaliana under a low phosphate (LP) condition. Root hair elongation under LP conditions was greatly suppressed in pin2 mutant or under treatment with a PLDζ2‐specific inhibitor, revealing that PIN2 and polar auxin transport and PLDζ2‐PA are crucial in LP responses. PIN2 was accumulated and degraded in the vacuole under a normal phosphate (NP) condition, whereas its vacuolar accumulation was suppressed under the LP or NP plus PA conditions. Vacuolar accumulation of PIN2 was increased in pldζ2 mutants under LP conditions. Increased or decreased PIN2 vacuolar accumulation is not observed in sorting nexin1 (snx1) mutant, indicating that vacuolar accumulation of PIN2 is mediated by SNX1 and the relevant trafficking process. PA binds to SNX1 and promotes its accumulation at the plasma membrane, especially under LP conditions, and hence promotes root hair development by suppressing the vacuolar degradation of PIN2. We uncovered a link between PLD‐derived PA and SNX1‐dependent vacuolar degradation of PIN2 in regulating root hair development under phosphorus deficiency.

Many studies have revealed that SPX (SYG1/Pho81/XPR1) family genes play a key role in signal transduction related to phosphorus (P) deficiency in plants. Here, we identified 33 SPX gene family members in maize through genome-wide analysis and classified them into 4 subfamilies according to SPX structural characteristics (SPX, SPX-MFS, SPX-EXS and SPX-RING). The promoter regions of ZmSPXs are rich in biotic/abiotic-related stress elements. The quantitative real-time PCR analysis of 33 ZmSPXs revealed that all members except for ZmSPX3 of the SPX subfamily were significantly induced under P-deficient conditions, especially ZmSPX4.1 and ZmSPX4.2, which showed strong responses to low P stress and exhibited remarkably different expression patterns in low Pi sensitive and insensitive cultivars of maize. These results suggested that the SPX subfamily might play pivotal roles in P stress sensing and response. Experimental observations of subcellular localization in maize protoplasts indicated the following results, implying multiple roles in cell metabolism: ZmSPX2, ZmSPX5 and ZmSPX6 localized in the nucleus; ZmSPX1 and ZmSPX3 localized in the nucleus and cytoplasm; and ZmSPX4.2 localized in the chloroplast. A Y2H assay suggested that ZmPHR1 could interact with ZmSPX3, ZmSPX4.2, ZmSPX5, and ZmSPX6, indicating the involvement of these proteins in the P stress response in a ZmPHR1-mediated manner.

Viruses often usurp host machineries for their amplification, but it remains unclear if hosts may subvert virus proteins to regulate viral proliferation. Here, we show that the 17K protein, an important virulence factor conserved in barley yellow dwarf viruses (BYDVs) and related poleroviruses, is phosphorylated by host GRIK1‐SnRK1 kinases, with the phosphorylated 17K (P17K) capable of enhancing the abundance of virus‐derived small interfering RNAs (vsiRNAs) and thus antiviral RNAi. Furthermore, P17K interacts with barley small RNA‐degrading nuclease 1 (HvSDN1) and impedes HvSDN1‐catalyzed vsiRNA degradation. Additionally, P17K weakens the HvSDN1‐HvAGO1 interaction, thus hindering HvSDN1 from accessing and degrading HvAGO1‐carried vsiRNAs. Importantly, transgenic expression of 17K phosphomimetics (17K^5D), or genome editing of SDN1, generates stable resistance to BYDV through elevating vsiRNA abundance. These data validate a novel mechanism that enhances antiviral RNAi through host subversion of a viral virulence protein to inhibit SDN1‐catalyzed vsiRNA degradation and suggest new ways for engineering BYDV‐resistant crops.