Disease Resistance in Plants that Carry a Feedback-regulated Yeast Poly(A) Binding Protein Gene

Abstract

It has been reported that the expression of the yeast poly(A) binding protein gene (PAB1) in plants leads to an induction of disease resistance responses, accompanied by alterations in the growth habit of the plant (Li et al. Plant Mol. Biol. (2000) 42 335). To capitalize on this observation, a feedback-regulated PAB1 gene was assembled and introduced into tobacco and Arabidopsis. The regulation entailed the linking of the expression of the PAB1 gene to control by the lac repressor, and by linking lac repressor expression to the disease resistance state of the plant, such that the induction of systemic defense responses by accumulation of the yeast poly(A) binding protein would turn off the expression of the PAB1 gene. Plants containing this system showed elevated and/or constitutive expression of disease-associated genes and significant resistance to otherwise pathogenic organisms. As well, they displayed a nearly normal growth habit under laboratory and greenhouse settings. These studies indicate that the expression of cytotoxic genes (such as the PAB1 gene) in plants can be controlled so that enhanced disease resistance can be achieved without significantly affecting plant growth and development.

The MAX2‐KAI2 module promotes salicylic acid‐mediated immune responses in Arabidopsis

“…To decipher the mechanism of MAX2‐mediated disease resistance, we retrieved information about the TF genes from the published literature. TGA3, MYB96, SARD1, CBP60g, and BT4 have been described as positive regulators (Kesarwani et al, 2007; Seo and Park, 2010; Wang et al, 2011; Zheng et al, 2019), whereas WRKY33, WRKY54, WRKY70, WRKY48, WRKY28, WRKY60, ATAF1 (ANAC2), and MYC2 are negative regulators of resistance to Pst DC3000 (Addepalli et al, 2006; Zheng et al, 2006; Ge et al, 2007; Xing et al, 2008; Charron et al, 2009; Birkenbihl et al, 2012; Davis et al, 2017). WRKY33, WRKY54, and WRKY70 have less of an effect on resistance to Pst DC3000 compared with other pathogens (Zheng et al, 2006; Xing et al, 2008; Davis et al, 2017).…”