Evaluating putative lncRNA ‐mediated ceRNA regulatory network involving miR396 and miR319 in maize leaf growth under Fusarium verticillioides infection

Abstract Fusarium verticillioides is a mycotoxigenic fungal pathogen of maize, causing seedling blight disease leading to impaired leaf growth, which is maintained by cell division and expansion mechanisms. MicroRNAs (miRNAs) and long non‐coding RNAs are main regulators of gene expression that are hypothesised to interact within a competitive endogenous RNA (ceRNA) regulatory network by competing for shared miRNA binding sites. This study evaluated the contribution of ceRNA networks to leaf growth regulation in response to F. verticillioides infection in tolerant (R) and susceptible (S) maize genotypes subjected to soil inoculation. The results showed that the final leaf length (FLL) shortened by 26% and 16% in the infected S and R lines, respectively, due to reduced cell division rate (D) by 31% in S line and shorter cell expansion time by 13% in R. Two potential ceRNA regulatory networks, miR396‐ GRF15 ‐lnc396 (ceR396) and miR319‐ TCP ‐lnc319 (ceR319), were predicted bioinformatically and their expression was determined in growth zones in response to infection. As a result, the expression level of lnc396 reduced by 0.5‐fold while miR396 and GRF15 remained unchanged in the infected meristem tissue of S line. However, miR319 was downregulated by 0.3‐fold, but its predicted target TCP38 was upregulated by 2‐fold in the infected meristem of R. Antioxidant enzyme assays revealed 3‐ and 2‐fold increase in ascorbate peroxidase and catalase activities, respectively, in the meristem of R line. These findings have contributed to knowledge on genotype‐dependent leaf growth response in maize under F. verticillioides attack through redox homeostasis and putative ceRNA network regulation.