The Arabidopsis Phosphatidylinositol-phospholipase C2 (AtPLC2) is involved in the flagellin-induced defense responses.

D'AMBROSSIO, JUAN MARTÍN; SCUFFI, DENISE; LAMATTINA, LORENZO; LAXALT, ANA MARÍA

Fos de Iguazú

Congreso; 11th International Congress of Plant Molecular Biology; 2015

IPMB

Plants are constantly exposed to pathogenic microorganisms. These can be detected by plant cells through recognition of microbe-associated molecular patterns (MAMPs) such as flagellin and chitin, triggering the ?non-host resistance? immunity against non-adapted pathogens. After recognition, a series of rapid responses are initiated. Several lipids and lipid metabolites have been shown to function in the signal transduction pathway leading to the activation of plant defense responses. The activation of Phosphatidylinositol-phospholipase C (PI-PLC) and the resulting accumulation of the lipid phosphatidic acid (PA) is one of the earliest host responses as evidenced upon treatment with several MAMPs. It is well documented that PI-PLC activation induces downstream plant defense responses. The Arabidopsis PI-PLC gene family is composed of 9 members. In particular, AtPLC2 is phosphorylated in vivo upon flagellin treatment, suggesting AtPLC2 might be involved in plant defense responses. The aim of this study is to asses the role of AtPLC2 during flagellin perception by means of reverse genetics. We silenced the expression of AtPLC2 through the constitutive expression of a specific artificial microRNAs in planta. Expression analysis of the PLC gene family in T3 homozygotes revealed that the silencing of AtPLC2 was specific and stable. These plant lines showed reduced flagellin-induced reactive oxygen species (ROS) production and callose deposition. In addition, the flagellin-mediated induction of stomatal closure was impaired in epidermal peels of AtPLC2-silenced plants, whereas the induction of stomatal closure by ABA was not affected. These results support the participation of AtPLC2 in the signaling of MAMPs triggered immunity (MTI).