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Expression GWAS of PGIP1 Identifies STOP1-Dependent and STOP1-Independent Regulation of PGIP1 in Aluminum Stress Signaling in Arabidopsis.

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.

SUBMITTER: Agrahari RK

PROVIDER: S-EPMC8719490 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Acidic soils constrain plant growth and development in natural and agricultural ecosystems because of the combination of multiple stress factors including high levels of Fe3+, toxic levels of Al3+, low phosphate (Pi) availability and proton rhizotoxicity. The transcription factor SENSITIVE TO PROTON RHIZOTOXICITY (STOP1) has been reported to underlie root adaptation to low pH, Al3+ toxicity and low Pi availability by activating the expression of genes involved in organic acid exudation, regulation of pH homeostasis, Al3+ detoxification and root architecture remodeling in Arabidopsis thaliana. However, the mechanisms by which STOP1 integrates these environmental signals to trigger adaptive responses to variable conditions in acidic soils remain to be unraveled. It is unknown whether STOP1 activates the expression of a single set of genes that enables root adaptation to acidic soils or multiple gene sets depending on the combination of different types of stress present in acidic soils. Previous transcriptomic studies of stop1 mutants and wild-type plants analyzed the effect of individual types of stress prevalent in acidic soils. An integrative study of the transcriptional regulation pathways that are activated by STOP1 under the combination of major stresses common in acidic soils is lacking. Using RNA-seq, we performed a transcriptional dissection of wild-type and stop1 root responses, individually or in combination, to toxic levels of Al3+, low Pi availability, low pH and Fe excess. We show that the level of STOP1 is post-transcriptionally and coordinately upregulated in the roots of seedlings exposed to single or combined stress factors. The accumulation of STOP1 correlates with the transcriptional activation of stress-specific and common gene sets that are activated in the roots of wild-type seedlings but not in stop1. Our data indicate that perception of low Pi availability, low pH, Fe excess and Al toxicity converges at two levels via STOP1 signaling: post-translationally through the regulation of STOP1 turnover, and transcriptionally, via the activation of STOP1-dependent gene expression that enables the root to better adapt to abiotic stress factors present in acidic soils.

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Expression GWAS of PGIP1 Identifies STOP1-Dependent and STOP1-Independent Regulation of PGIP1 in Aluminum Stress Signaling in Arabidopsis.

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