Abstract
Coprinopsis cinerea lectin 2 (CCL2) is a fucoside-binding lectin from the basidiomycete C. cinerea that is toxic to the bacterivorous nematode Caenorhabditis elegans as well as animal-parasitic and fungivorous nematodes. We expressed CCL2 in Arabidopsis to assess its protective potential toward plant-parasitic nematodes. Our results demonstrate that expression of CCL2 enhances host resistance against the cyst nematode Heterodera schachtii. Surprisingly, CCL2-expressing plants were also more resistant to fungal pathogens including Botrytis cinerea, and the phytopathogenic bacterium Pseudomonas syringae. In addition, CCL2 expression positively affected plant growth indicating that CCL2 has the potential to improve two important agricultural parameters namely biomass production and general disease resistance. The mechanism of the CCL2-mediated enhancement of plant disease resistance depended on fucoside-binding by CCL2 as transgenic plants expressing a mutant version of CCL2 (Y92A), compromised in fucoside-binding, exhibited wild type (WT) disease susceptibility. The protective effect of CCL2 did not seem to be direct as the lectin showed no growth-inhibition toward B. cinerea in in vitro assays. We detected, however, a significantly enhanced transcriptional induction of plant defense genes in CCL2- but not CCL2-Y92A-expressing lines in response to infection with B. cinerea compared to WT plants. This study demonstrates a potential of fungal defense lectins in plant protection beyond their use as toxins.
Highlights
Plants are exposed to a wide range of biotic stress caused by numerous pathogens and pests
This study demonstrates that expression of Coprinopsis cinerea lectin 2 (CCL2) in Arabidopsis plants enhances disease resistance against the sugar beet cyst nematode Heterodera schachtii, three fungal pathogens and the phytopathogenic bacterium Pseudomonas syringae
Quantification of rosettes of 4-week-old plants indicated that fresh weight (FW) and dry weight (DW) were significantly higher in transgenic plants (Figures 1D,E)
Summary
Plants are exposed to a wide range of biotic stress caused by numerous pathogens and pests. The first layer, pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI), is activated by the perception of PAMPs such as chitin oligomers or bacterial flagellin via pattern recognition receptors at the cell surface (Jones and Dangl, 2006; Schwessinger and Zipfel, 2008). A local inoculation with a potential pathogen or treatment with specific chemical compounds enhances disease resistance of the whole plant against a wide range of pathogens. This is achieved by the local activation of signal transduction pathways that lead to the systemic induction of plant immune responses (Pieterse et al, 2012)
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