Journal
PLANT CELL
Volume 24, Issue 4, Pages 1654-1674Publisher
AMER SOC PLANT BIOLOGISTS
DOI: 10.1105/tpc.112.096768
Keywords
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Funding
- National Science Foundation [EPS 0236913, MCB 0455318, MCB 0920663, DBI 0521587, 051909, 0749731]
- K-IDeA Networks of Biomedical Research Excellence of the National Institutes of Health [P20RR16475]
- Direct For Biological Sciences [1051909] Funding Source: National Science Foundation
- Direct For Biological Sciences
- Div Of Molecular and Cellular Bioscience [0920663] Funding Source: National Science Foundation
- Division Of Integrative Organismal Systems [1051909] Funding Source: National Science Foundation
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The conserved cellular metabolites nitric oxide (NO) and oleic acid (18: 1) are well-known regulators of disease physiologies in diverse organism. We show that NO production in plants is regulated via 18:1. Reduction in 18: 1 levels, via a genetic mutation in the 18: 1-synthesizing gene SUPPRESSOR OF SA INSENSITIVITY OF npr1-5 (SSI2) or exogenous application of glycerol, induced NO accumulation. Furthermore, both NO application and reduction in 18: 1 induced the expression of similar sets of nuclear genes. The altered defense signaling in the ssi2 mutant was partially restored by a mutation in NITRIC OXIDE ASSOCIATED1 (NOA1) and completely restored by double mutations in NOA1 and either of the nitrate reductases. Biochemical studies showed that 18:1 physically bound NOA1, in turn leading to its degradation in a protease-dependent manner. In concurrence, overexpression of NOA1 did not promote NO-derived defense signaling in wild-type plants unless 18: 1 levels were lowered. Subcellular localization showed that NOA1 and the 18: 1 synthesizing SSI2 proteins were present in close proximity within the nucleoids of chloroplasts. Indeed, pathogen-induced or low-18:1-induced accumulation of NO was primarily detected in the chloroplasts and their nucleoids. Together, these data suggest that 18: 1 levels regulate NO synthesis, and, thereby, NO-mediated signaling, by regulating NOA1 levels.
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