Silencing COI1 in Rice Increases Susceptibility to Chewing Insects and Impairs Inducible Defense

The jasmonic acid (JA) pathway plays a key role in plant defense responses against herbivorous insects. CORONATINE INSENSITIVE1 (COI1) is an F-box protein essential for all jasmonate responses. However, the precise defense function of COI1 in monocotyledonous plants, especially in rice (Oryza sativa L.) is largely unknown. We silenced OsCOI1 in rice plants via RNA interference (RNAi) to determine the role of OsCOI1 in rice defense against rice leaf folder (LF) Cnaphalocrocis medinalis, a chewing insect, and brown planthopper (BPH) Nilaparvata lugens, a phloem-feeding insect. In wild-type rice plants (WT), the transcripts of OsCOI1 were strongly and continuously up-regulated by LF infestation and methyl jasmonate (MeJA) treatment, but not by BPH infestation. The abundance of trypsin protease inhibitor (TrypPI), and the enzymatic activities of polyphenol oxidase (PPO) and peroxidase (POD) were enhanced in response to both LF and BPH infestation, but the activity of lipoxygenase (LOX) was only induced by LF. The RNAi lines with repressed expression of OsCOI1 showed reduced resistance against LF, but no change against BPH. Silencing OsCOI1 did not alter LF-induced LOX activity and JA content, but it led to a reduction in the TrypPI content, POD and PPO activity by 62.3%, 48.5% and 27.2%, respectively. In addition, MeJA-induced TrypPI and POD activity were reduced by 57.2% and 48.2% in OsCOI1 RNAi plants. These results suggest that OsCOI1 is an indispensable signaling component, controlling JA-regulated defense against chewing insect (LF) in rice plants, and COI1 is also required for induction of TrypPI, POD and PPO in rice defense response to LF infestation

Regulation and Role of Arabidopsis CUL4-DDB1A-DDB2 in Maintaining Genome Integrity upon UV Stress

Plants use the energy in sunlight for photosynthesis, but as a consequence are exposed to the toxic effect of UV radiation especially on DNA. The UV-induced lesions on DNA affect both transcription and replication and can also have mutagenic consequences. Here we investigated the regulation and the function of the recently described CUL4-DDB1-DDB2 E3 ligase in the maintenance of genome integrity upon UV-stress using the model plant Arabidopsis. Physiological, biochemical, and genetic evidences indicate that this protein complex is involved in global genome repair (GGR) of UV-induced DNA lesions. Moreover, we provide evidences for crosstalks between GGR, the plant-specific photo reactivation pathway and the RAD1-RAD10 endonucleases upon UV exposure. Finally, we report that DDB2 degradation upon UV stress depends not only on CUL4, but also on the checkpoint protein kinase Ataxia telangiectasia and Rad3-related (ATR). Interestingly, we found that DDB1A shuttles from the cytoplasm to the nucleus in an ATR-dependent manner, highlighting an upstream level of control and a novel mechanism of regulation of this E3 ligase

Suppression of Jasmonic Acid-Dependent Defense in Cotton Plant by the Mealybug Phenacoccus solenopsis

The solenopsis mealybug, Phenacoccus solenopsis, has been recently recognized as an aggressively invasive pest in China, and is now becoming a serious threat to the cotton industry in the country. Thus, it is necessary to investigate the molecular mechanisms employed by cotton for defending against P. solenopsis before the pest populations reach epidemic levels. Here, we examined the effects of exogenous jasmonic acid (JA), salicylic acid (SA), and herbivory treatments on feeding behavior and on development of female P. solenopsis. Further, we compared the volatile emissions of cotton plants upon JA, SA, and herbivory treatments, as well as the time-related changes in gossypol production and defense-related genes. Female adult P. solenopsis were repelled by leaves from JA-treated plant, but were not repelled by leaves from SA-treated plants. In contrast, females were attracted by leaves from plants pre-infested by P. solenopsis. The diverse feeding responses by P. solenopsis were due to the difference in volatile emission of plants from different treatments. Furthermore, we show that JA-treated plants slowed P. solenopsis development, but plants pre-infested by P. solenopsis accelerated its development. We also show that P. solenopsis feeding inhibited the JA-regulated gossypol production, and prevented the induction of JA-related genes. We conclude that P. solenopsis is able to prevent the activation of JA-dependent defenses associated with basal resistance to mealybugs

Tomato Pathogenesis-related Protein Genes are Expressed in Response to Trialeurodes vaporariorum and Bemisia tabaci Biotype B Feeding

The temporal and spatial expression of tomato wound- and defense-response genes to Bemisia tabaci biotype B (the silverleaf whitefly) and Trialeurodes vaporariorum (the greenhouse whitefly) feeding were characterized. Both species of whiteflies evoked similar changes in tomato gene expression. The levels of RNAs for the methyl jasmonic acid (MeJA)- or ethylene-regulated genes that encode the basic β-1,3-glucanase (GluB), basic chitinase (Chi9), and Pathogenesis-related protein-1 (PR-1) were monitored. GluB and Chi9 RNAs were abundant in infested leaves from the time nymphs initiated feeding (day 5). In addition, GluB RNAs accumulated in apical non-infested leaves. PR-1 RNAs also accumulated after whitefly feeding. In contrast, the ethylene- and salicylic acid (SA)-regulated Chi3 and PR-4 genes had RNAs that accumulated at low levels and GluAC RNAs that were undetectable in whitefly-infested tomato leaves. The changes in Phenylalanine ammonia lyase5 (PAL5) were variable; in some, but not all infestations, PAL5 RNAs increased in response to whitefly feeding. PAL5 RNA levels increased in response to MeJA, ethylene, and abscisic acid, and declined in response to SA. Transcripts from the wound-response genes, leucine aminopeptidase (LapA1) and proteinase inhibitor 2 (pin2), were not detected following whitefly feeding. Furthermore, whitefly infestation of transgenic LapA1:GUS tomato plants showed that whitefly feeding did not activate the LapA1 promoter, although crushing of the leaf lamina increased GUS activity up to 40 fold. These studies indicate that tomato plants perceive B. tabaci and T. vaporariorum in a manner similar to baterical pathogens and distinct from tissue-damaging insects

Signal interactions in pathogen and insect attack: Systemic plant-mediated interactions between pathogens and herbivores of the tomato, Lycopersicon esculentum

Plant-mediated interactions (i.e., induced resistance) between plant pathogens and insect herbivores were investigated using several pests of the cultivated tomato, Lycopersicon esculentum. Single leaflets of tomato leaves were injured by allowing a third-instar Helicoverpa zea larva to feed on the leaflets or by inoculating the leaflets with Pseudomonas syringae pv. tomato (the causal agent of bacterial speck in tomato; Pst) or with Phytophthora infestans (the causal agent of late blight). Leaflets on separate plants were sprayed with benzothiadiazole, a chemical inducer of resistance to Psi. The effects of these treatments on the resistance of uninoculated or undamaged leaflets to both Pst and H. zea were then assessed after appropriate periods of time. The levels or activities of several defense-related proteins were determined in parallel. Infection of leaflets by Pst decreased the suitability of uninoculated leaflets of the same leaf for both H. zea and for Pst. Similarly, feeding by H. zea caused leaf-systemic increases in resistance to both H. zea and Pst. Infection of leaflets by P. infestans, in contrast, had no effect on resistance of leaflets to H. zea. Treatment of leaves with benzothiadiazole induced resistance to Pst but improved suitability of leaflets for H. zea. Feeding by H. zea caused the systemic accumulation of proteinase inhibitor mRNA and the systemic induction of polyphenol oxidase activity; in contrast, treatment with benzothiadiazole and inoculation with P. infestans caused the systemic accumulation of pathogenesis-related protein mRNA and the systemic induction of peroxidase activity. Inoculation of leaflets with Pst caused the leaf-systemic accumulation of both pathogenesis-related protein and proteinase inhibitor mRNA and the systemic induction of both peroxidase and polyphenol oxidase activity. These results provide clear evidence for reciprocal induced resistance involving certain pathogens and arthropod herbivores of tomato. In addition, these results provide several insights into the integration and coordination of the induced defenses of tomato against multiple pests and suggest that the expression of resistance against some pests may compromise resistance to others

Signal interactions in pathogen and insect attack: Expression of lipoxygenase, proteinase inhibitor II, and pathogenesis-related protein P4 in the tomato, Lycopersicon esculentum

Pathogens and insects can elicit different sets of plant host responses, supporting the hypothesis for control by different signaling pathways. To evaluate the potential for signal interaction in plants attacked by pathogens and insects, the mRNA abundance for lipoxygenase (LOX), a wound-inducible proteinase inhibitor (PINII), and a pathogenesis-related protein (P4) was evaluated in tomato leaves following challenge with a variety of agents. PINII and P4 expression was determined as these proteins are induced in tomato leaves characteristically following attack by certain insects or pathogens, respectively. Expression studies of LOX, PINII, and P4 indicate that their induction in tomato does not follow a strict pattern based on the type of biologic inducer (insect vs. pathogen) or chemical treatment, with each specific treatment inducing a distinct pattern of gene expression. However, plants induced to express disease resistance with the synthetic salicylate mimic benzothiadiazole-7-carbothioic acid S-methyl ester were compromised in their expression of the wound- or jasmonate-activated PINII, consistent with an observed increase in susceptibility to insect herbivory reported in a companion study. The results do not support the hypothesis for a strict dichotomy of signaling by insects and pathogens of LOX, PINII and P4 in tomato, but point to a potential vulnerability of acquired resistance evident at the levels of gene expression and response to insect attack