Plant disease resistance is commonly triggered by early pathogen recognition and activation of immunity. An alternative form of resistance is mediated by recessive downy mildew resistant 1 (dmr1) alleles in Arabidopsis thaliana. Map-based cloning revealed that DMR1 encodes homoserine kinase (HSK). Six independent dmr1 mutants each carry a different amino acid substitution in the HSK protein. Amino acid analysis revealed that dmr1 mutants contain high levels of homoserine that is undetectable in wild-type plants. Surprisingly, the level of amino acids downstream in the aspartate (Asp) pathway was not reduced in dmr1 mutants. Exogenous homoserine does not directly affect pathogen growth but induces resistance when infiltrated in Arabidopsis. We provide evidence that homoserine accumulation in the chloroplast triggers a novel form of downy mildew resistance that is independent of known immune responses.

Abstract-NO deficiency is associated with development of hypertension. Defects in the renal citrulline-arginine pathway or arginine reabsorption potentially reduce renal NO in prehypertensive spontaneously hypertensive rats (SHRs). Hence, we investigated genes related to the citrulline-arginine pathway or arginine reabsorption, amino acid pools, and renal NO in 2-week-old prehypertensive SHRs. In addition, because perinatally supporting NO availability reduces blood pressure in SHRs, we supplemented SHR dams during pregnancy and lactation with citrulline, the rate-limiting amino acid for arginine synthesis. In female offspring, gene expression of argininosuccinate synthase (involved in renal arginine synthesis) and renal cationic amino acid Y-transporter (involved in arginine reabsorption) were both decreased in 2-day and 2-week SHRs compared with normotensive WKY, although no abnormalities in amino acid pools were observed. In addition, 2-week-old female SHRs had much less NO in their kidneys (0.46Ϯ0.01 versus 0.68Ϯ0.05 nmol/g of kidney weight, respectively; PϽ0.001) but not in their heart. Furthermore, perinatal supplementation with citrulline increased renal NO to 0.59Ϯ0.02 nmol/g of kidney weight (PϽ0.001) at 2 weeks and persistently ameliorated the development of hypertension in females and until 20 weeks in male SHR offspring. Defects in both the renal citrulline-arginine pathway and in arginine reabsorption precede hypertension in SHRs. We propose that the reduced cationic amino acid transporter disables the developing SHR kidney to use arginine reabsorption to compensate for reduced arginine synthesis, resulting in organ-specific NO deficiency. This early renal deficiency and its adverse sequels can be corrected by perinatal citrulline supplementation persistently in female and transiently in male SHRs. Key Words: NO Ⅲ amino acids Ⅲ hypertension Ⅲ developmental plasticity Ⅲ electron paramagnetic resonance Ⅲ citrulline H ypertension is associated with oxidative stress, often caused by a self-perpetuating cycle of NO deficiency, increased reactive oxygen species, and a disturbed constrictor-dilator balance in the kidney. 1 Inhibition of NO synthase (NOS) causes marked and persistent hypertension. [2][3][4] Therefore, an impairment of the NO-generating pathway could be involved in the onset of hereditary hypertension. It is even conceivable that a reduction in renal NO precedes hypertension.There are multiple causes of a reduced or deficient NO generation in the prehypertensive kidney. Among others, these are reduced availability of NOS or the NOS substrate L-arginine. In this regard, Vaziri et al 5 reported an abundance of NOS isoforms in kidneys of juvenile spontaneously hypertensive rats (SHRs). Using microarray methodology, we identified a reduction in the expression of argininosuccinate synthase (ASS) and the arginine transporter slc7a7 in kidneys of young SHRs. This led us to investigate the challenging issue of whether NO deficiency precedes hypertension because of reduced arginine availability in SH...