Acid soil syndrome causes severe yield losses in various crop plants because of the rhizotoxicities of ions, such as aluminum (Al 3؉ ). Although protons (H ؉ ) could be also major rhizotoxicants in some soil types, molecular mechanisms of their tolerance have not been identified yet. One mutant that was hypersensitive to H ؉ rhizotoxicity was isolated from ethyl methanesulfonate mutagenized seeds, and a single recessive mutation was found on chromosome 1. Positional cloning followed by genomic sequence analysis revealed that a missense mutation in the zinc finger domain in a predicted Cys2His2-type zinc finger protein, namely sensitive to proton rhizotoxicity (STOP)1, is the cause of hypersensitivity to H ؉ rhizotoxicity. The STOP1 protein belongs to a functionally unidentified subfamily of zinc finger proteins, which consists of two members in Arabidopsis based on a Blast search. The stop1 mutation resulted in no effects on cadmium, copper, lanthanum, manganese and sodium chloride sensitivitities, whereas it caused hypersensitivity to Al 3؉ rhizotoxicity. This stop1 mutant lacked the induction of the AtALMT1 gene encoding a malate transporter, which is concomitant with Al-induced malate exudation. There was no induction of AtALMT1 by Al 3؉ treatment in the stop1 mutant. These results indicate that STOP1 plays a critical role in Arabidopsis tolerance to major stress factors in acid soils. aluminum toxicity ͉ Arabidopsis thaliana ͉ Cys2His2-type zinc finger protein ͉ proton-rhizotoxicity ͉ sensitive to proton rhizotoxicity

SummaryArabidopsis carries three receptor genes for the phytohormone gibberellin (GA), AtGID1a, AtGID1b and AtGID1c. Expression of each gene in the rice gid1-1 mutant for GA receptors causes reversion of its severely dwarfed phenotype and GA insensitivity to a normal level, even though each loss-of-function mutant shows no clear phenotype in Arabidopsis (Nakajima et al., 2006). In this paper, we report the functional redundancy and specificity of each AtGID1 by analyzing the multiple mutants for loss of function. Seeds of the double knockout mutants atgid1a atgid1b, atgid1a atgid1c and atgid1b atgid1c germinated normally. The double knockout mutant atgid1a atgid1c showed a dwarf phenotype, while other double mutants were of normal height compared to the wild-type. The stamens of the double knockout mutant atgid1a atgid1b were significantly shorter than those of the wild-type, and this leads to low fertility. A severe disarrangement of the pattern on its seed surface was also observed. The triple knockout mutant atgid1a atgid1b atgid1c did not germinate voluntarily, and only started to grow when the seed coat was peeled off after soaking. Seedlings of the triple knockout mutants were severe dwarfs, only a few millimeters high after growing for 1 month. Moreover, the triple knockout seedlings completely lost their ability to respond to exogenously applied GA. These results show that all AtGID1s function as GA receptors in Arabidopsis, but have specific role(s) for growth and development.

Botrytis cinerea is a ubiquitous necrotrophic fungal pathogen that infects over 200 different plant species. We have analyzed 17 Arabidopsis ecotypes for natural variations in their susceptibility to B. cinerea, and found compatible and incompatible Arabidopsis-Botrytis interactions. We determined that Arabidopsis ecotype Ler is resistant to 5 B. cinerea isolates used in this study. To further investigate the roles of the salicylic acid (SA)-dependent defense response pathways against B. cinerea, we inoculated various Arabidopsis mutants with the pathogen. Arabidopsis Ler plants expressing the nahG gene inoculated with B. cinerea showed as much resistance as the parental plants (Ler-wild type). The sgt1b-1 and rar1-10 mutants also showed resistance to the pathogen. In this study, we discuss the natural variations in the symptoms observed among various ecotypes upon inoculation with B. cinerea. In addition, SA plays only a minor role in preventing systemic infection with B. cinerea.