Further analyses show that PSTOL1 acts as an enhancer of early root growth, thereby enabling plants to acquire more phosphorus and other nutrients. The absence of PSTOL1 and other genes—for example, the submergence-tolerance gene SUB1A—from modern rice varieties underlines the importance of conserving and exploring traditional germplasm. Introgression of this quantitative trait locus into locally adapted rice varieties in Asia and Africa is expected to considerably enhance productivity under low phosphorus conditions.
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Guests: Dr. Jeffery Dangl, John N. Couch Professor of Biology, HHMI/GBMF investigator, Department of Biology, UNC-Chapel Hill, and Dr. Sarah Grant, Research Associate Professor, Department of Biology, UNC-Chapel Hill Topics: Plant microbiomes, plant immune systems, development of the Arabidopsis thaliana plant model, importance of plant biology, science policy
Plant activators are compounds, such as analogs of the defense hormone salicylic acid (SA), that protect plants from pathogens by activating the plant immune system. Although some plant activators have been widely used in agriculture, the molecular mechanisms of immune induction are largely unknown. Using a newly established high-throughput screening procedure that screens for compounds that speciﬁcally potentiate pathogen-activated cell death in Arabidopsis thaliana cultured suspension cells, we identiﬁed ﬁve compounds that prime the immune response. These compounds enhanced disease resistance against pathogenic Pseudomonas bacteria in Arabidopsis plants. Pretreatments increased the accumulation of endogenous SA, but reduced its metabolite, SA-O-b-D-glucoside. Inducing compounds inhibited two SA glucosyltransferases (SAGTs) in vitro. Double knockout plants that lack both SAGTs consistently exhibited enhanced disease resistance. Our results demonstrate that manipulation of the active free SA pool via SA-inactivating enzymes can be a useful strategy for fortifying plant disease resistance and may identify useful crop protectants.
Yoshiteru Noutoshi, Masateru Okazaki, Tatsuya Kida, Yuta Nishina, Yoshihiko Morishita, Takumi Ogawa, Hideyuki Suzuki, Daisuke Shibata, Yusuke Jikumaru, Atsushi Hanada, Yuji Kamiya, and Ken Shirasu
Panicle blast 1 (Pb1) encodes a coiled-coil–nucleotide-binding site–leucine-rich repeat (CC-NB-LRR) protein and confers durable, broad-spectrum resistance to Magnaporthe oryzae races. The Pb1 protein interacted with WRKY45, a transcription factor involved in induced resistance via the salicylic acid signaling pathway that is regulated by the ubiquitin proteasome system. Pb1-mediated panicle blast resistance was largely compromised when WRKY45 was knocked down in a Pb1-containing rice cultivar. Leaf-blast resistance by Pb1 overexpression (Pb1-ox) was also compromised in WRKY45 knockdown/Pb1-ox rice. These results suggest that the blast resistance of Pb1 depends on its interaction with WRKY45 in the nucleus.
Pathogens target important components of host immunity to cause disease. The Pseudomonas syringae type III-secreted effector HopU1 is a mono-ADP-ribosyltransferase required for full virulence on Arabidopsis thaliana. HopU1 targets several RNA-binding proteins including GRP7, whose role in immunity is still unclear. Here, we show that GRP7 associates with translational components, as well as with the pattern recognition receptors FLS2 and EFR. Moreover, GRP7 binds specifically FLS2 and EFR transcripts in vivo through its RNA recognition motif. HopU1 does not affect the protein–protein associations between GRP7, FLS2 and translational components. Instead, HopU1 blocks the interaction between GRP7 and FLS2 and EFR transcripts in vivo. This inhibition correlates with reduced FLS2 protein levels upon Pseudomonas infection in a HopU1-dependent manner. Our results reveal a novel virulence strategy used by a microbial effector to interfere with host immunity.
The results indicated that the PTS1 peroxisomal import pathway, in addition to PTS2, is required for fungal development and pathogenicity of the rice blast fungus, and also, as a main peroxisomal import pathway, played a more predominant role than PTS2.
The level of JA-isoleucine (JA-Ile), a bioactive form of jasmonate, increased in response to blast infection. Furthermore, blast-induced accumulation of phytoalexins, especially that of the flavonoid sakuranetin, was found to be severely impaired in cpm2 and hebiba. Together, the present study demonstrates that in rice jasmonate mediates the defence response against blast fungus.
The AvrPiz-t gene encodes a small protein predicted to be secreted that shows no homology to known proteins and is 108 amino acids in length. AvrPiz-t can suppress programmed cell death (PCD) induced by BAX in tobacco, suggesting that it might contribute to the pathogenicity of M. oryzae. These data suggested that AvrPiz-t functions primarily as a virulence effector contributing to the pathogenicity of M. oryzae. To further understand the mechanism of the pathogenicity-associated function of AvrPiz-t, we determined its solution structure.
Typically, pathogens deploy virulence effectors to disable defense. Plants defeat effectors with resistance proteins that guard effector targets. Here, we show that a pathogen exploits a resistance protein by activating it to confer susceptibility. Interactions of victorin, an effector produced by the necrotrophic fungusCochliobolus victoriae, TRX-h5, a defense-associated thioredoxin, and LOV1, an Arabidopsis susceptibility protein, recapitulate the guard mechanism of plant defense. In LOV1's absence, victorin inhibits TRX-h5 resulting in compromised defense but not disease by C. victoriae. In LOV1's presence, victorin binding to TRX-h5 activates LOV1 and elicits a resistance-like response that confers disease susceptibility. We propose that victorin is or mimics a conventional pathogen virulence effector that was defeated by LOV1 and confers virulence to C. victoriae solely because it incites defense.
Does the Arabidopsis receptor FLS2 respond to CLV3 and Ax21 peptides? "The editors of The Plant Cell feel that they have taken responsibility for opening up the scientific debate on FLS2 and innate immune signaling, and they have gone as far as possible to ensure a fair and balanced discussion of issues of particular interest to its readership":
Katharina Mueller, Delphine Chinchilla, Markus Albert, Anna K. Jehle, Hubert Kalbacher, Thomas Boller, and Georg Felix. Contamination Risks in Work with Synthetic Peptides: flg22 as an Example of a Pirate in Commercial Peptide Preparations http://tinyurl.com/c2u3pr6
Cécile Segonzac, Zachary L. Nimchuk, Martina Beck, Paul T. Tarr, Silke Robatzek, Elliot M. Meyerowitz, and Cyril Zipfel. The Shoot Apical Meristem Regulatory Peptide CLV3 Does Not Activate Innate Immunity http://tinyurl.com/bslnq4o
Horim Lee, Ashok Khatri, Julia M. Plotnikov, Xue-Cheng Zhang, and Jen Sheen. Complexity in Differential Peptide–Receptor Signaling: Response to Segonzac et al. and Mueller et al. Commentaries http://tinyurl.com/c2csqm3
Cristian H. Danna, Xue-Cheng Zhang, Ashok Khatri, Andrew F. Bent, Pamela C. Ronald, and Frederick M. Ausubel. FLS2-Mediated Responses to Ax21-Derived Peptides: Response to the Mueller et al. Commentary http://tinyurl.com/d2a36cr