The zinc-finger protein STOP1 (sensitive to proton rhizotoxicity 1) regulates transcription of multiple genes critical for tolerance to aluminum (Al) and low pH in Arabidopsis. We evaluated the contributions of genes that are suppressed in the stop1 mutant to Al- and low pH-tolerance using T-DNA-inserted disruptants, and transgenic stop1 mutants expressing each of the suppressed genes. STOP2, a STOP1 homolog, partially recovered Al- and low pH-tolerance by recovering the expression of genes regulated by STOP1. Growth and root tip viability under proton stress were partially rescued in the STOP2-complemented line. STOP2 localized in the nucleus and regulated transcription of two genes (PGIP1 and PGIP2) associated with cell wall stabilization at low pH. GUS assays revealed that STOP1 and STOP2 showed similar cellular expression in the root. However, the expression level of STOP2 was much lower than that of STOP1. In a STOP1 promoter::STOP2-complemented line, Al tolerance was slightly recovered, concomitant with the recovery of expression of ALS3 (aluminum sensitive 3) and AtMATE (Arabidopsis thaliana multidrug and toxic compound extrusion), while the expression of AtALMT1 (aluminum-activated malate transporter 1) was not recovered. These analyses indicated that STOP2 is a physiologically minor isoform of STOP1, but it can activate expression of some genes regulated by STOP1.

Plants have evolved a series of tolerance mechanisms to saline stress, which perturbs physiological processes throughout the plant. To identify genetic mechanisms associated with salinity tolerance, we performed linkage analysis and genome-wide association study (GWAS) on maintenance of root growth of Arabidopsis thaliana in hydroponic culture with weak and severe NaCl toxicity. The top 200 single-nucleotide polymorphisms (SNPs) determined by GWAS could cumulatively explain approximately 70% of the variation observed at each stress level. The most significant SNPs were linked to the genes of ATP-binding cassette B10 and vacuolar proton ATPase A2. Several known salinity tolerance genes such as potassium channel KAT1 and calcium sensor SOS3 were also linked to SNPs in the top 200. In parallel, we constructed a gene co-expression network to independently verify that particular groups of genes work together to a common purpose. We identify molecular mechanisms to confer salt tolerance from both predictable and novel physiological sources and validate the utility of combined genetic and network analysis. Additionally, our study indicates that the genetic architecture of salt tolerance is responsive to the severity of stress. These gene datasets are a significant information resource for a following exploration of gene function.

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To understand mechanisms of cadmium (Cd) tolerance variation associated with root elongation in Arabidopsis thaliana, quantitative trait loci (QTLs) and epistasis were analyzed using relative root length (RRL: % of the root length in +Cd to -Cd) as a tolerant index. Using the composite interval mapping method, three major QTLs (P < 0.05) were detected on chromosomes 2, 4 and 5 in the recombinant inbred population derived from a cross between Landsberg erecta (Ler-0) and Columbia (Col-4). The highest logarithm of odds (LOD) of 5.6 was detected with the QTL on chromosome 5 (QTL5), which is linked to the genetic marker CDPK9 and explained about 26% of the Cd tolerance variation. There was no significant difference in Cd-translocation ratio from roots to shoots between tolerant and sensitive recombinant inbreed lines (RILs), while greater accumulations of reactive oxygen species were observed in the roots of sensitive RILs. This suggested that accumulation of ROS would explain Cd tolerance variation of the Ler/Col RILs, which is mainly controlled by the QTL on chromosome 5. The QTL5 in Ler/Col population was also detected as one of the major QTLs controlling tolerances to hydrogen peroxide and to copper, which is another ROS generating rhizotoxic metal. The same chromosomal position was detected as a common major QTL for Cd and hydrogen peroxide tolerances in a different recombinant inbreed (RI) population derived from a cross of Col-gl1 and Kashmir (Kas-1). These data, along with a multitraits QTL analysis in both sets of RILs, suggest that peroxide damage depends on the genotype at a major Cd-tolerant locus on the upper part of chromosome 5.

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