A Methyl Viologen-Resistant Mutant of Arabidopsis, Which Is Allelic to Ozone-Sensitive rcd1, Is Tolerant to Supplemental Ultraviolet-B Irradiation

Abstract

To better understand the role of active oxygen species (AOS) in acquired resistance to increased levels of ultraviolet (UV)-B irradiation in plants, we isolated an Arabidopsis mutant that is resistant to methyl viologen, and its sensitivity to UV-B was investigated. A complementation test revealed that the obtained mutant was allelic to the ozone-sensitive radical-induced cell death1-1 (rcd1-1). Therefore, this mutant was named rcd1-2. rcd1-2 was recessive and nearly 4-fold more resistant to methyl viologen than wild type. It exhibited a higher tolerance to short-term UV-B supplementation treatments than the wild type: UV-B-induced formation of cyclobutane pyrimidine dimers was reduced by one-half after 24 h of exposure; the decrease in quantum yield of photosystem II was also diminished by 40% after 12 h of treatment. Furthermore, rcd1-2 was tolerant to freezing. Steady-state mRNA levels of plastidic Cu/Zn superoxide dismutase and stromal ascorbate peroxidase were higher in rcd1-2 than in wild type, and the mRNA level of the latter enzyme was enhanced by UV-B exposure more effectively in rcd1-2. UV-B-absorbing compounds were more accumulated in rcd1-2 than in wild type after UV-B exposure for 24 h. These findings suggest that rcd1-2 methyl viologen resistance is due to the enhanced activities of the AOS-scavenging enzymes in chloroplasts and that the acquired tolerance to the short-term UV-B exposure results from a higher accumulation of sunscreen pigments. rcd1 appears to be a mutant that constitutively shows stress responses, leading to accumulation of more pigments and AOS-scavenging enzymes without any stresses.

The Arabidopsis PARAQUAT RESISTANT2 gene encodes an S-nitrosoglutathione reductase that is a key regulator of cell death

“…Consistently, chloroplasttargeted overexpression of superoxide dismutase (SOD) genes confers paraquat resistance in a number of transgenic species [19][20][21]. Interestingly, the Arabidopsis radical-induced cell death1 (rcd1) mutant displays resistance to paraquat, and this phenotype is associated with the increased expression of plastidic Cu/Zn SOD and ascorbate peroxidase (APX) genes [22]. These results suggest that paraquat-induced cell death is mediated by a ROS-based signaling pathway.…”

“…One possibility is the detoxifying effect such as by the removal of excessive amount of ROS and reactive hydroxyl radicals. The Arabidopsis rcd1 mutant, for example, displays resistance to paraquat, and this phenotype is associated with the increased expression of plastidic SOD and APX genes [22]. Similarly, the paraquat-induced cell death can also be suppressed by overexpression of a chloroplast-targeted SOD gene [20] or a thylakoidal APX gene [51].…”

The Paralogous GenesRADICAL-INDUCED CELL DEATH1andSIMILAR TO RCD ONE1Have Partially Redundant Functions during Arabidopsis Development

“…rcd1 mutants display accumulation of both ethylene and salicylic acid and altered expression of ethyleneand abscisic acid-responsive genes (Ahlfors et al, 2004). In addition, rcd1 plants are hypersensitive to ozone (Overmyer et al, 2005) and conversely are resistant to UV-B light (Fujibe et al, 2004). The phenotypic analysis suggests that RCD1 may be a convergence point for several hormone signaling pathways involved in the stress response and act both negatively and positively in stress responses (Ahlfors et al, 2004).…”

“…It is involved in the response to several abiotic stresses, including ozone. All rcd1 alleles confer dominant ozone hypersensitivity, although they seem to be recessive for other phenotypes (Ahlfors et al, 2004;Fujibe et al, 2004). rcd1 mutants display accumulation of both ethylene and salicylic acid and altered expression of ethyleneand abscisic acid-responsive genes (Ahlfors et al, 2004).…”

Mitogen-Activated Protein Kinases and Reactive Oxygen Species Signaling in Plants

“…Further evidence for the involvement of MAPKs in the ozone response comes from analyses of the ozonesensitive radical-induced cell death 1 (rcd1) mutant; ozoneinduced cell death in rcd1 was blocked by diphenylene iodonium (Overmyer et al, 2000), an inhibitor of NADPH oxidases, and rcd1 mutants display enhanced resistance toward methyl viologen (Fujibe et al, 2004). Furthermore, ozone-exposed rcd1 have increased salicylic acid levels and show earlier activation of MPK6 compared to wild-type plants (Overmyer et al, 2005).…”