Abstract
The Arabidopsis rugosa1 (rug1) mutant has irregularly shaped leaves and reduced growth. In the absence of pathogens, leaves of rug1 plants have spontaneous lesions reminiscent of those seen in lesion-mimic mutants; rug1 plants also express cytological and molecular markers associated with defence against pathogens. These rug1 phenotypes are made stronger by dark/light transitions. The rug1 mutant also has delayed flowering time, upregulation of the floral repressor FLOWERING LOCUS C (FLC) and downregulation of the flowering promoters FT and SOC1/AGL20. Vernalization suppresses the late flowering phenotype of rug1 by repressing FLC. Microarray analysis revealed that 280 nuclear genes are differentially expressed between rug1 and wild type; almost a quarter of these genes are involved in plant defence. In rug1, the auxin response is also affected and several auxin-responsive genes are downregulated. We identified the RUG1 gene by map-based cloning and found that it encodes porphobilinogen deaminase (PBGD), also known as hydroxymethylbilane synthase, an enzyme of the tetrapyrrole biosynthesis pathway, which produces chlorophyll, heme, siroheme and phytochromobilin in plants. PBGD activity is reduced in rug1 plants, which accumulate porphobilinogen. Our results indicate that Arabidopsis PBGD deficiency impairs the porphyrin pathway and triggers constitutive activation of plant defence mechanisms leading to leaf lesions and affecting vegetative and reproductive development.
Highlights
Lesion-mimic mutants, which spontaneously develop necrotic leaf lesions similar to those caused by pathogen attack, have been identified in Arabidopsis thaliana and other plant species [1,2]
In Nicotiana tabacum, lesion mimic phenotypes are caused by RNA interferencemediated repression of coproporphyrinogen III oxidase (CPO) [11,12], urophorphyrinogen decarboxylase III (UROD) [12,13], protoporphyrinogen IX oxidase (PPO) [14] and FeCh [15]
Confocal microscopy and examination of transverse sections revealed that internal leaf structure was extremely perturbed in rug1: the lesion sectors lacked the chlorophyll autofluorescence normally exhibited by mesophyll cells (Figure 2c, f, h, i) and contained large air spaces (Figure 2h–k)
Summary
Lesion-mimic mutants, which spontaneously develop necrotic leaf lesions similar to those caused by pathogen attack, have been identified in Arabidopsis thaliana and other plant species [1,2]. Several mutations causing lesion-mimic phenotypes have been cloned and some of these genes encode tetrapyrrole biosynthesis enzymes. Antisense-RNA mediated inhibition of genes encoding tetrapyrrole biosynthesis enzymes, such as the Arabidopsis glutamyl-tRNA reductase (GluTR; Figure 1) [9], and protoporphyrinogen IX oxidase (PPO; Figure 1) [10], can cause lesion mimic phenotypes. In Nicotiana tabacum, lesion mimic phenotypes are caused by RNA interferencemediated repression of CPO [11,12], UROD [12,13], PPO [14] and FeCh (ferrochelatase, an enzyme that acts in the heme branch of the tetrapyrrole biosynthesis pathway) [15]
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