We used a survey of attendees of an organic farming conference in Minnesota, U.S.A., to determine whether farmers would be more likely to adopt a fall-seeded winter rye cover crop preceding soybeans if doing so could aid in the suppression of soybean aphid, Aphis glycines Matsumura (Homoptera: Aphididae). Of the 24 soybean growers that responded to our survey, 22 indicated that they would be more likely to either adopt or retain this cover cropping practice if it could aid in soybean aphid suppression. Insect pest suppression may therefore be an effective way to augment adoption of cover cropping practices. INTRODUCTION Fall-seeded winter cover crops have the potential to improve soil organic matter, reduce soil erosion, manage excess nutrient loads, and provide for weed and insect management. While the benefits of cover crops to soil fertility, nutrient scavenging, and erosion and weed control are well-documented, research showing improvement in insect control has lagged behind in many cover-cropping systems. To illustrate this, we did a literature search on the AGRICOLA database to compare the number of scientific citations associated with cover crops and terms associated with ‘soil’, ‘weeds’ and ‘insects’. There was a clear deficit of citations associated with the term ‘insects’ and ‘insect control’ when paired with ‘cover crop’ (Table 1).
The rice blast fungus Magnaporthe oryzae is a model for studying fungal–plant interactions. Although it produces two types of spores (microconidia and macroconidia), previous infection studies have exclusively dealt with macroconidia. Germination of microconidia has not been reported, and their role in plant infection is not defined. Here we show that approximately 10% of microconidia germinate on plant surfaces, and that colonies derived from germinated microconidia are normal in growth and pathogenesis. In infection assays with rice and barley seedlings, microconidia fail to infect intact plants, but they can colonize and develop necrotic lesions on wounded leaves and stems. Microconidia also cause disease symptoms on inoculated spikelets in infection assays with barley and Brachypodium heads. Furthermore, microconidia are detected inside rice plants that developed blast lesions under laboratory or field conditions. Therefore, microconidia can germinate and are infectious, and may be an important factor in the rice blast cycle. The rice blast fungus Magnaporthe oryzae produces large and small spores, and the role played by the small spores (microconidia) in plant infection is unknown. Here, Zhang et al.show that the microconidia can cause disease by infecting plants through wounds or flowering heads.
Abstract The H3 methyltransferases ATXR5 and ATXR6 deposit H3.1K27me1 to heterochromatin to prevent genomic instability and transposon re-activation. Here, we report that atxr5 atxr6 mutants display robust resistance to Geminivirus. The viral resistance is correlated with activation of DNA repair pathways, but not with transposon re-activation or heterochromatin amplification. We identify RAD51 and RPA1A as partners of virus-encoded Rep protein. The two DNA repair proteins show increased binding to heterochromatic regions and defense-related genes in atxr5 atxr6 vs wild-type plants. Consequently, the proteins have reduced binding to viral DNA in the mutant, thus hampering viral amplification. Additionally, RAD51 recruitment to the host genome arise via BRCA1, HOP2, and CYCB1;1, and this recruitment is essential for viral resistance in atxr5 atxr6 . Thus, Geminiviruses adapt to healthy plants by hijacking DNA repair pathways, whereas the unstable genome, triggered by reduced H3.1K27me1, could retain DNA repairing proteins to suppress viral amplification in atxr5 atxr6 .
Abstract Plant immune responses are mainly activated by two types of receptors. Plasma membrane-localized pattern recognition receptors (PRRs) recognize conserved features of microbes, and intracellular nucleotide-binding leucine rich repeat receptors (NLRs) recognize effector proteins from pathogens. NLRs possessing N-terminal Toll/interleukin-1 receptor (TIR) domains (TNLs) activate two parallel signaling pathways via the EDS1/PAD4/ADR1s and the EDS1/SAG101/NRG1s modules. The relationship between PRR-mediated pattern-triggered immunity (PTI) and TIR signaling is unclear. Here we report that activation of TIR signaling plays a key role in PTI. Blocking TIR signaling by knocking out components of the EDS1/PAD4/ADR1s and EDS1/SAG101/NRG1s modules results in attenuated PTI responses such as reduced salicylic acid (SA) levels and expression of defense genes, and compromised resistance against pathogens. Consistently, PTI is attenuated in transgenic plants that have reduced accumulation of NLRs. Upon treatment with PTI elicitors such as flg22 and nlp20, a large number of genes encoding TNLs or TIR domain-containing proteins are rapidly induced, likely responsible for activating TIR signaling during PTI. In support, overexpression of some of these genes results in activation of defense responses. Overall, our study reveals that TIR signaling activation is an important mechanism for boosting plant defense during PTI.
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