Abstract
In Fabaceae, dispersion of forisomes-highly ordered aggregates of sieve element proteins-in response to phytoplasma infection was proposed to limit phloem mass flow and, hence, prevent pathogen spread. In this study, the involvement of filamentous sieve element proteins in the containment of phytoplasmas was investigated in non-Fabaceae plants. Healthy and infected Arabidopsis plants lacking one or two genes related to sieve element filament formation-AtSEOR1 (At3g01680), AtSEOR2 (At3g01670), and AtPP2-A1 (At4g19840)-were analysed. TEM images revealed that phytoplasma infection induces phloem protein filament formation in both the wild-type and mutant lines. This result suggests that, in contrast to previous hypotheses, sieve element filaments can be produced independently of AtSEOR1 and AtSEOR2 genes. Filament presence was accompanied by a compensatory overexpression of sieve element protein genes in infected mutant lines in comparison with wild-type lines. No correlation was found between phloem mass flow limitation and phytoplasma titre, which suggests that sieve element proteins are involved in defence mechanisms other than mechanical limitation of the pathogen.
Highlights
Phytoplasmas are prokaryotic plant pathogens belonging to the class Mollicutes
We investigated if phytoplasma-triggered sieve element (SE) protein filament presence really limits the phloem flow and if this strategy can eventually limit pathogen capability to proliferate in phloem tissue
These findings led to the hypothesis that SE filaments are involved in plant response to pathogen attack and, under stress conditions, their formation becomes independent of the presence of AtSEOR1 or AtSEOR2
Summary
Phytoplasmas are prokaryotic plant pathogens belonging to the class Mollicutes. They are transferred by insect vectors to the phloem, where they exercise their pathogenic influence on the plant (Lee et al, 2000; Bertaccini and Duduk, 2009; Bertaccini et al, 2014). Phytoplasma outbreak and spread can only be controlled by using insecticides. Alternative strategies, such as the individuation of resistant or tolerant plants (Osler et al, 2014, 2016), require a thorough notion of the physiological mechanisms underlying the interactions between plant host and phytoplasmas
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