Project description:MicroRNAs (miRNAs) are small non-coding RNAs that function as post-transcriptional regulators of gene expression in eukaryotes. In rice, miR7695 targets an alternatively spliced transcript of natural resistance-associated macrophage protein 6 (OsNramp6) encoding an iron transporter whose expression is regulated by infection with the rice blast fungus Magnaporthe oryzae. Rice plants grown under high iron supply showed blast resistance, which supports that iron is a factor in controlling blast resistance by still unknown mechanisms. Here, iron accumulated near M. oryzae appressoria, the sites of pathogen entry, and in cells surrounding infected regions of the rice leaf. Activation-tagged MIR7695 rice plants (MIR7695-Ac) exhibited enhanced resistance to M. oryzae infection. RNA-seq analysis revealed that blast resistance in MIR7695-Ac plants was associated with strong induction of defense-related genes, including pathogenesis-related and diterpenoid biosynthetic genes. Levels of phytoalexins during pathogen infection were higher in MIR7695-Ac than wild-type plants. Early phytoalexin biosynthetic genes, OsCPS2 and OsCSP4, were highly upregulated in rice plants grown under high iron supply. Our data indicate that miR7695 positively regulates rice immunity while establishing links between defense and iron signaling in rice. MiR7695-mediated regulation of OsNramp6 has great potential for the development of strategies to control rice blast disease.
Project description:Improvement of chilling tolerance is a key strategy to face potential menace from abnormal temperature in rice production, which depends on the signaling network triggered by receptors. However, little is known about the QTL genes encoding membrane complexes for sensing cold. Here, Chilling-tolerance in Gengdao/japonica rice 1 (COG1) was isolated from a chromosome segment substitution line containing a QTL (qCS11-jap) for chilling sensitivity. The major gene COG1 was found to confer chilling tolerance in japonica rice. In natural rice populations, only the haplogroup1 encoded a functional COG1. Evolutionary analysis showed that COG1 originated from Chinese O. Rufipogon and was fixed in japonica rice during domestication. COG1, a membrane-localized LRR-RLP, targeted and activated the kinase OsSERL2 in a cold-induced manner, promoting chilling tolerance. Furthermore, the cold signal transmitted by COG1-OsSERL2 activates OsMAPK3 in the cytoplasm. Our findings reveal a cold-sensing complex, which mediates signaling network for the chilling defense in rice.
Project description:In rice, a number of resistance (R) genes that counter the blast fungus, Magnaporthe oryzae, have been cloned, but the mechanism by which they trigger disease resistance remains elusive. This is in part due to a lack of comprehensive transcriptome analyses during the resistance or disease progression. Here, we monitored the gene expression profiling in rice during its interactions with Magnaporthe by time-series transcriptome analyses. Distinct from previous studies, we focused on early infection stages within 24 hours post-inoculation. A comparison of those expression changes revealed a general difference in gene expression kinetics between compatible and incompatible interactions, and pointed to that the time when the pathogen just establishes its penetration into rice cells is a key point for the expressional changes. Such conclusions originated from the R gene Pid3-mediated immune responses were validated in the R gene Pi9-mediated responses, suggesting common molecular processes are shared by different R-mediated blast immunity. Our data highlighted the role of jasmonic acid (JA)-triggered signaling pathway (JA pathway) in the hormone signaling network for rice blast resistance. We confirmed that both exogenous and endogenous JA can induce the expression of many defense-related components revealed in above transcriptomic analyses and proved that the knock-down of OsCOI1 which encodes a JA receptor may deprive rice of the blast resistance mediated by R genes. Therefore, it is concluded that JA pathway plays an essential role in the establishment of blast resistance by modulating the expression of other defense-related components.
Project description:Rice blast disease is a major threat to rice production worldwide, but the mechanisms underlying rice resistance to the causal agent Magnaporthe oryzae remain elusive. In this whole-genome transcriptome study of rice early defense response to M. oryzae, we applied Affymetrix Rice Genome Genechip to compare the compatible and incompatible rice-M. oryzae interactions in 24 hours post-inoculation.
Project description:Nucleotide-binding site leucine-rich repeat (NLR) receptors perceive pathogen effectors and trigger plant immunity. However, the mechanisms underlying NLR-triggered defense responses remain obscure. The recently discovered Pigm locus in rice encodes a cluster of NLRs, including PigmR, which confers broad-spectrum resistance to blast fungus. Here, we identify PIBP1 (PigmR-INTERACTING and BLAST RESISTANCE PROTEIN 1), an RRM (RNA-recognition motif) protein that specifically interacts with PigmR and other similar NLRs to trigger blast resistance. PigmR-promoted nuclear accumulation of PIBP1 ensures full blast resistance. We find that PIBP1 and a homolog, Os06 g02240, bind DNA and function as unconventional transcription factors at the promoters of the defense genes OsWAK14 and OsPAL1, activating their expression. Knockout of PIBP1 and Os06g02240 greatly attenuated blast resistance. Collectively, our study discovers previously unappreciated RRM transcription factors that directly interact with NLRs to activate plant defense, establishing a direct link between transcriptional activation of immune responses with NLR-mediated pathogen perception
Project description:Nucleotide-binding site leucine-rich repeat (NLR) receptors perceive pathogen effectors and trigger plant immunity. However, the mechanisms underlying NLR-triggered defense responses remain obscure. The recently discovered Pigm locus in rice encodes a cluster of NLRs, including PigmR, which confers broad-spectrum resistance to blast fungus. Here, we identify PIBP1 (PigmR-INTERACTING and BLAST RESISTANCE PROTEIN 1), an RRM (RNA-recognition motif) protein that specifically interacts with PigmR and other similar NLRs to trigger blast resistance. PigmR-promoted nuclear accumulation of PIBP1 ensures full blast resistance. We find that PIBP1 and a homolog, Os06 g02240, bind DNA and function as unconventional transcription factors at the promoters of the defense genes OsWAK14 and OsPAL1, activating their expression. Knockout of PIBP1 and Os06g02240 greatly attenuated blast resistance. Collectively, our study discovers previously unappreciated RRM transcription factors that directly interact with NLRs to activate plant defense, establishing a direct link between transcriptional activation of immune responses with NLR-mediated pathogen perception
Project description:Nucleotide-binding site leucine-rich repeat (NLR) receptors perceive pathogen effectors and trigger plant immunity. However, the mechanisms underlying NLR-triggered defense responses remain obscure. The recently discovered Pigm locus in rice encodes a cluster of NLRs, including PigmR, which confers broad-spectrum resistance to blast fungus. Here, we identify PIBP1 (PigmR-INTERACTING and BLAST RESISTANCE PROTEIN 1), an RRM (RNA-recognition motif) protein that specifically interacts with PigmR and other similar NLRs to trigger blast resistance. PigmR-promoted nuclear accumulation of PIBP1 ensures full blast resistance. We find that PIBP1 and a homolog, Os06 g02240, bind DNA and function as unconventional transcription factors at the promoters of the defense genes OsWAK14 and OsPAL1, activating their expression. Knockout of PIBP1 and Os06 g02240 greatly attenuated blast resistance. Collectively, our study discovers previously unappreciated RRM transcription factors that directly interact with NLRs to activate plant defense, establishing a direct link between transcriptional activation of immune responses with NLR-mediated pathogen perception.
Project description:Phosphorus (P) is an essential nutrient for plant growth and productivity. Due to soil fixation, however, phosphorus availability in soil is rarely sufficient to sustain high crop yields. Fertilizers are widely used to circumvent the limited bioavailability of phosphate (Pi) which led to a scenario of excessive soil P in agricultural soils. Whereas adaptive responses to Pi deficiency have been deeply studied, less is known about how plants adapt to Pi excess and how Pi excess might affect disease resistance. Here, we show that high Pi fertilization in rice plants, and subsequent Pi accumulation in leaves, enhances susceptibility to infection by Magnaporthe oryzae, the causal agent of the rice blast disease. Equally, MIR399f overexpression causes an increase in Pi content in rice leaves which results in enhanced susceptibility to M. oryzae. During pathogen infection, a weaker activation of defense-related genes occurs in rice plants accumulating Pi in leaves, a response that is in agreement with the phenotype of blast susceptibility observed in these plants. These data support that Pi, when in excess, compromises defense mechanisms in rice while demonstrating that miR399 functions as a negative regulator of rice immunity. The two signaling pathways, Pi signaling and defense signaling, must operate in a coordinated manner in controlling disease resistance. This information provides a basis to understand the molecular mechanisms involved in immunity in rice plants grown under a high Pi fertilization regime, an aspect that should be considered in management of the rice blast disease