Plasmodesmal closure elicits stress responses

Abstract

Plant cells are connected to their neighbors via plasmodesmata facilitating the exchange of nutrients, hormones, and signaling molecules. While immune elicitors trigger changes in plasmodesmal aperture, it is unknown how this contributes towards a full immune response. To investigate this, we developed two transgenic lines with which we could induce plasmodesmal closure independently of immune elicitors. Thus, we used the over-active CALLOSE SYNTHASE3 allele icals3m and the C-terminus of PDLP1 to drive callose deposition at plasmodesmata in response to estradiol treatment. These lines showed different degrees of plasmodesmal closure but both showed upregulation of the expression of stress responsive genes, the accumulation of salicylic acid and enhanced resistance to Pseudomonas syringae DC3000 in response to estradiol treatment. Enhanced resistance was not correlated with perturbation of the flg22-triggered ROS burst or MAPK signaling. Enhanced plasmodesmal closure using icals3m also led to the measurable accumulation of starch and sugars, decreased leaf growth, and induced leaf senescence. Additionally, induction of plasmodesmal closure using icals3m led to hypersusceptibility to Botrytis cinerea. We conclude that plasmodesmal closure itself can activate stress signaling, raising questions of how this occurs, what signal carries this information and whether these responses occur in all circumstances when plasmodesmata close across plant physiology.