AUTHOR=Lu Pan-Pan , Yu Tai-Fei , Zheng Wei-Jun , Chen Ming , Zhou Yong-Bin , Chen Jun , Ma You-Zhi , Xi Ya-Jun , Xu Zhao-Shi 

TITLE=The Wheat Bax Inhibitor-1 Protein Interacts with an Aquaporin TaPIP1 and Enhances Disease Resistance in Arabidopsis

JOURNAL=Frontiers in Plant Science

VOLUME=9

YEAR=2018

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2018.00020

DOI=10.3389/fpls.2018.00020

ISSN=1664-462X

ABSTRACT=<p>Bax inhibitor-1 (BI-1) is an endoplasmic reticulum (ER)-resident cell death suppressor evolutionarily conserved in eukaryotes. The ability of BI-1 to inhibit the biotic and abiotic stresses have been well-studied in <italic>Arabidopsis</italic>, while the functions of wheat BI-1 are largely unknown. In this study, the wheat BI-1 gene <italic>TaBI-1.1</italic> was isolated by an RNA-seq analysis of <italic>Fusarium graminearum</italic> (<italic>Fg</italic>)-treated wheat. <italic>TaBI-1.1</italic> expression was induced by a salicylic acid (SA) treatment and down-regulated by an abscisic acid (ABA) treatment. Based on β-glucuronidase (GUS) staining, <italic>TaBI-1.1</italic> was expressed in mature leaves and roots but not in the hypocotyl or young leaves. Constitutive expression of <italic>TaBI-1.1</italic> in <italic>Arabidopsis</italic> enhanced its resistance to <italic>Pseudomonas syringae</italic> pv. <italic>Tomato</italic> (<italic>Pst</italic>) DC3000 infection and induced SA-related gene expression. Additionally, <italic>TaBI-1.1</italic> transgenic <italic>Arabidopsis</italic> exhibited an alleviation of damage caused by high concentrations of SA and decreased the sensitivity to ABA. Consistent with the phenotype, the RNA-seq analysis of <italic>35S::TaBI-1.1</italic> and Col-0 plants showed that <italic>TaBI-1.1</italic> was involved in biotic stresses. These results suggested that <italic>TaBI-1.1</italic> positively regulates SA signals and plays important roles in the response to biotic stresses. In addition, TaBI-1.1 interacted with the aquaporin TaPIP1, and both them were localized to ER membrane. Furthermore, we demonstrated that <italic>TaPIP1</italic> was up-regulated by SA treatment and <italic>TaPIP1</italic> transgenic <italic>Arabidopsis</italic> enhanced the resistance to <italic>Pst</italic> DC3000 infection. Thus, the interaction between TaBI-1.1 and TaPIP1 on the ER membrane probably occurs in response to SA signals and defense response.</p>