Epigenetic Switches in the Proximal 3' UTR Reprograms TaFAR1-L Temporal Expression in Wheat During Leaf Rust...

Noncoding DNA sequences within the genome are often overlooked as a source of cellular regulatory information. Here, we examined the regulatory role of the proximal 3' UTR sequence of FAR-RED IMPAIRED RESPONSE1 (FAR1) and the epigenetic modifications within this region, which contribute to the regulation of gene expression of FAR1. FAR1 is a transcription factor derived from transposase, which has a crucial role in light signaling and defense responses during environmental constraints. Since the comprehensive identification of FAR1 and the investigation of its regulatory responses in wheat has not been conducted yet, our examination focused on the deciphering of its importance during leaf rust pathogenesis in susceptible (HD2329) and resistant (HD2329 + Lr24) near isogenic lines of wheat. We identified 19 TaFAR1-L homoeologs, gene copies across the wheat A, B, and D subgenomes, through a genome mining search. Additionally, leaf rust (Puccinia triticina) responsive miRNAs targeting these TaFAR1-L genes were identified and their interaction networks were analyzed. Their phylogenetic relationship with Arabidopsis thaliana and related monocots (Sorghum bicolor, Brachypodium distachyon, Hordeum vulgare, and Zea mays) were also studied. Also, the methylation states of the CpG sites within their cis-regulatory elements at the 3' UTR (300 bp downstream CDS) of one of the homoeologous genes, TaFAR1-L-15, were identified. We report a significant demethylation of these CpG dinucleotides in the resistant near isogenic line after 24 h post inoculation, followed up by their synergistic upregulated expression and the antagonistic downregulated leaf rust-responsive miRNA TamiR 142 expression. However, contrasting results were obtained for the susceptible near isogenic line. Thus, our findings indicate that TaFAR1-L might act as a positive regulator of leaf rust tolerance. Moreover, cytosine methylation at proximal 3' UTR cis-elements could potentially serve as a marker or lever for controlling TaFAR1-L expression.