Local and systemic regulation of PSII efficiency in triticale infected by the hemibiotrophic pathogen Microdochium nivale.

Abstract

Microdochium nivale is a fungal pathogen that causes yield losses of cereals during winter. Cold hardening under light conditions induces genotype-dependent resistance of a plant to infection. We aim to show how photosystem II (PSII) regulation contributes to plant resistance. Using mapping population of triticale doubled haploid lines, three M. nivale strains and different infection assays, we demonstrate that plants that maintain a higher maximum quantum efficiency of PSII show less leaf damage upon infection. The fungus can establish necrotrophic or biotrophic interactions with susceptible or resistant genotypes, respectively. It is suggested that local inhibition of photosynthesis during the infection of sensitive genotypes is not balanced by a supply of energy from the tissue surrounding the infected cells as efficiently as in resistant genotypes. Thus, defence is limited, which in turn results in extensive necrotic damage. Quantitative trait loci regions, involved in the control of both PSII functioning and resistance, were located on chromosomes 4 and 6, similar to a wide range of PSII- and resistance-related genes. A meta-analysis of microarray experiments showed that the expression of genes involved in the repair and de novo assembly of PSII was maintained at a stable level. However, to establish a favourable energy balance for defence, genes encoding PSII proteins resistant to oxidative degradation were downregulated to compensate for the upregulation of defence-related pathways. Finally, we demonstrate that the structural and functional integrity of the plant is a factor required to meet the energy demand of infected cells, photosynthesis-dependent systemic signalling and defence responses.