Abstract

Many aspects of interactions between grapevine yellows phytoplasmas (GYP) and their grapevine hosts remain unclear. However, based on the available data, it appears that damage caused by GYP to their hosts is greater than might be expected from their relatively low titre in the phloem and their uneven distribution throughout the plant. Moreover, it is hard to define the limits between the common plant responses to an infection and the real GYP activities towards obtaining the necessary compounds for their life within the host. Collective evidence suggests that the accumulation of soluble carbohydrates in GYP-infected plants results in feedback inhibition of photosynthesis, which causes a source–sink transition. In many microbe–plant interactions, cell-wall invertase, which hydrolyses sucrose to glucose and fructose, plays an important role in disease expression. However, it appears that in the grapevine–GYP interaction, another enzyme has a leading function, sucrose synthase, on the basis of providing both fructose for the GYP and UDP-glucose for the plant responses to the infection. In parallel to the responses of the genes involved in primary carbohydrate metabolism, sink-specific secondary metabolism pathways that involve genes and metabolites of the shikimic acid and oxidative pentose phosphate pathway are induced, along with genes involved in direct defence responses. The observed changes in metabolism of GYP-infected plants suggest that infected grapevines respond to this pathogen through induced salicylic-acid-dependent systemic acquired resistance.

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