Abstract
To elucidate the unknown regulatory mechanisms involved in aluminum (Al)-induced expression of POLYGALACTURONASE-INHIBITING PROTEIN 1 (PGIP1), which is one of the downstream genes of SENSITIVE TO PROTON RHIZOTOXICITY 1 (STOP1) regulating Al-tolerance genes, we conducted a genome-wide association analysis of gene expression levels (eGWAS) of PGIP1 in the shoots under Al stress using 83 Arabidopsis thaliana accessions. The eGWAS, conducted through a mixed linear model, revealed 17 suggestive SNPs across the genome having the association with the expression level variation in PGIP1. The GWAS-detected SNPs were directly located inside transcription factors and other genes involved in stress signaling, which were expressed in response to Al. These candidate genes carried different expression level and amino acid polymorphisms. Among them, three genes encoding NAC domain-containing protein 27 (NAC027), TRX superfamily protein, and R-R-type MYB protein were associated with the suppression of PGIP1 expression in their mutants, and accordingly, the system affected Al tolerance. We also found the involvement of Al-induced endogenous nitric oxide (NO) signaling, which induces NAC027 and R-R-type MYB genes to regulate PGIP1 expression. In this study, we provide genetic evidence that STOP1-independent NO signaling pathway and STOP1-dependent regulation in phosphoinositide (PI) signaling pathway are involved in the regulation of PGIP1 expression under Al stress.
Highlights
In the last few decades, extensive studies in molecular physiological research for aluminum (Al) toxicity in acid soils have found that activation of Al-tolerance genes governs Al resistance in plants (Delhaize and Ryan, 1995; Liu et al, 2014; Kochian et al, 2015)
We examined the 12 candidate genes for expression level polymorphisms (ELPs) and amino acid polymorphisms associated with the POLYGALACTURONASE-INHIBITING PROTEIN 1 (PGIP1) expression level
TRX SF, R-R MYB, and NAC027 involved in the regulatory mechanisms of Al-inducible PGIP1 expression were identified through eGWAS of PGIP1 expression levels under Al stress (Figure 3; Table 1)
Summary
In the last few decades, extensive studies in molecular physiological research for aluminum (Al) toxicity in acid soils (pH < 5.5) have found that activation of Al-tolerance genes governs Al resistance in plants (Delhaize and Ryan, 1995; Liu et al, 2014; Kochian et al, 2015). Several transcription factors that activate the transcription of critical Al-resistant genes (ALMT1); Tokizawa et al, 2015) have been identified, including. Al-inducible expression of STOP1-regulated genes plays critical roles in Al tolerance in Arabidopsis (Sawaki et al., 2009) and is conserved in various plant species (Ohyama et al., 2013). It is important to identify the mechanisms regulating gene expression related to Al tolerance, which would be helpful in the field of breeding and the management of crops in acid soil. Several mechanisms regulating the expression of STOP1-. The expression of AtALMT1 under Al stress involves calcium signaling that includes CALCINEURIN B-LIKE PROTEIN 1
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