The Intergenic Interplay between and in Abiotic and Biotic Stress Control.

The mechanical damage that often precedes the penetration of a leaf by a pathogen promotes the activation of pectin methylesterase (PME); the activation of PME leads to the emission of methanol, resulting in a "priming" effect on intact leaves, which is accompanied by an increased sensitivity to (TMV) and resistance to bacteria. In this study, we revealed that mRNA levels of the methanol-inducible gene encoding aldose 1-epimerase-like protein (NbAELP) in the leaves of intact plants are very low compared with roots. However, stress and pathogen attack increased the accumulation of the mRNA in the leaves. Using transiently transformed plants, we obtained data to support the mechanism underlying AELP/PME-related negative feedback The insertion of the promoter sequence (proNbAELP) into the genome resulted in the co-suppression of the natural gene expression, accompanied by a reduction in the mRNA content and increased PME synthesis. Knockdown of resulted in high activity of PME in the cell wall and a decrease in the leaf glucose level, creating unfavorable conditions for reproduction in injected leaves. Our results showed that NbAELP is capable of binding the TMV movement protein (MP) and is likely to affect the cellular nucleocytoplasmic transport, which may explain the sensitivity of knockdown plants to TMV. Although NbAELP was primarily detected in the cell wall, the influence of this protein on cellular mRNA levels might be associated with reduced transcriptional activity of the gene in the nucleus. To confirm this hypothesis, we isolated the gene promoter (proNtPME) and showed the inhibition of proNtPME-directed and expression in leaves when co-agroinjected with the NbAELP-encoding plasmid. We hypothesized that plant wounding and/or pathogen attack lead to PME activation and increased methanol emission, followed by increased expression, which results in reversion of mRNA level and methanol emission to levels found in the intact plant.