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Mwimba, M.

Publications and source records attributed to Mwimba, M..

3 recordsLinked to original sources

Primary metabolism determines the outcome of salicylic acid-mediated immune induction

Controlling the deleterious effects of immune responses is as vital as fighting infection. In plants, this is achieved, in part, by circadian clock-mediated regulation, such as the synthesis of and response to the immune hormone salicylic acid (SA)1,2. Application of SA at the same concentration under light/dark cycles induces immunity with minimal impact on growth, however, prolonged darkness leads to plant death2. To uncover what determines this life-or-death outcome, we identified twenty survival of SA-induced death (ssd) mutants through genetic screening. These mutants are defective in starch, glucose, and nitrate metabolism, and circadian regulation, and accumulate excessive starch and/or glucose. Likewise, glucose application rescues SA-treated plants in prolonged darkness. Surprisingly, SA treatment does not deplete glucose, but instead, induces amino acid and fatty acid catabolism. Through transcriptomic analyses of glucose-rescued WT plants and ssd mutants for shared pathways, we found that SA triggers plant death in darkness by inducing oxidative stress, and water loss, while glucose antagonizes these processes, boosts ER protein processing and re-establishes the anabolism-catabolism balance. Interestingly, the programmed cell death induced by effector-triggered immunity shares common transcriptomic patterns with those observed during SA-induced cell death in darkness and could also be attenuated by glucose treatment. Therefore, coordination with the cellular metabolic context plays a central role in determining immune outcomes and optimizing plant health.

plant biology↗

H2O2 sulfenylates CHE linking local infection to establishment of systemic acquired resistance

In plants, a local infection can lead to systemic acquired resistance (SAR) through increased production of salicylic acid (SA). For 30 years, the identity of the mobile signal and its direct transduction mechanism for systemic SA synthesis in initiating SAR have been hotly debated. We found that, upon pathogen challenge, the cysteine residue of transcription factor CHE undergoes sulfenylation in systemic tissues, enhancing its binding to the promoter of SA-synthesis gene, ICS1, and increasing SA production. This occurs independently of previously reported pipecolic acid (Pip) signal. Instead, H2O2 produced by NADPH oxidase, RBOHD, is the mobile signal that sulfenylates CHE in a concentration-dependent manner. This modification serves as a molecular switch that activates CHE-mediated SA-increase and subsequent Pip-accumulation in systemic tissues to synergistically induce SAR. One Sentence SummaryRBOHD-generated H2O2 sulfenylates transcription factor CHE to establish systemic acquired resistance in plants.

plant biology↗

Circadian redox rhythm gates immune-induced cell death distinctly from the genetic clock

Organisms use circadian clocks to synchronize physiological processes to anticipate the Earths day-night cycles and regulate responses to environmental stresses to gain competitive advantage1. While divergent genetic clocks have been studied extensively in bacteria, fungi, plants, and animals, a conserved circadian redox rhythm has only recently been reported and hypothesized to be a more ancient clock2, 3. However, it is controversial whether the redox rhythm serves as an independent clock and controls specific biological processes4. Here, we uncovered the coexistence of redox and genetic rhythms with distinct period lengths and transcriptional targets through concurrent metabolic and transcriptional time-course measurements in an Arabidopsis long-period clock mutant5. Analysis of the target genes indicated regulation of the immune-induced programmed cell death (PCD) by the redox rhythm. Moreover, this time-of-day-sensitive PCD was eliminated by redox perturbation and by blocking the signalling pathway of the plant defence hormones jasmonic acid/ethylene, while remaining intact in a genetic-clock-impaired line. We demonstrate that compared to robust genetic clocks, the more sensitive circadian redox rhythm serves as a signalling hub in regulating incidental energy-intensive processes, such as immune-induced PCD6, to provide organisms a flexible strategy to prevent metabolic overload caused by stress, a unique role for the redox oscillator.

plant biology↗