Increased susceptibility to Chrysanthemum Yellows phytoplasma infection in Atcals7 ko plants is accompanied by enhanced expression of carbohydrate transporters

Abstract

Callose accumulation around sieve pores, under control of Callose synthase 7 (AtCALS7), has been interpreted as a mechanical response to limit pathogen spread in phytoplasma-infected plants. AtCALS7 is also involved in sieve-pore development and, hence, in mass-flow regulation, carbohydrate metabolism and distribution, and plant growth. Multiple roles of AtCALS7 during phytoplasma infection were investigated in healthy and phytoplasma-infected [Chrysanthemum Yellows (CY)-phytoplasma] wild-type and Atcals7ko Arabidopsis lines. In keeping with an increased phytoplasma titre in Atcals7ko plants, floral stalk height of infected wild-type and mutant plants was reduced by, respectively, 88 and 100% in comparison to their healthy controls, suggesting a higher investment of host resources in phytoplasma growth in the absence of AtCALS7. The apparently increased susceptibility of mutants was investigated by microscopic, metabolic and molecular analyses. Infection influenced the sieve-pore functionality in wild-type plants, which hardly affected plant growth, and plasmodesmata in the cortex, a phenomenon less prominent in mutants. Infection also increased the level of some sugars (glucose, sucrose, myoinositol), but to the highest extent in mutants. Finally, infection induced a similar upregulation of gene expression of enzymes involved in sucrose cleavage (AtSUS5, AtSUS6) in mutants and wild-type plants and an upregulation of carbohydrate transmembrane transporters (AtSWEET11, AtSTP13, AtSUC3) in mutants only. A more effective plasmodesmal closure seemingly suppressed spread of phytoplasma effectors, which rendered wild-type plants less susceptible to infection, because gene expression of enzymes channeling carbohydrates towards phytoplasmas is less promoted