RESUMEN
Plasma membrane (PM) depolarization functions as an initial step in plant defense signaling pathways. However, only a few ion channels/transporters have been characterized in the context of plant immunity. Here, we show that the Arabidopsis (Arabidopsis thaliana) Na+:K+:2Cl- (NKCC) cotransporter CCC1 has a dual function in plant immunity. CCC1 functions independently of PM depolarization and negatively regulates pathogen-associated molecular pattern-triggered immunity. However, CCC1 positively regulates plant basal and effector-triggered resistance to Pseudomonas syringae pv. tomato (Pst) DC3000. In line with the compromised immunity to Pst DC3000, ccc1 mutants show reduced expression of genes encoding enzymes involved in the biosynthesis of antimicrobial peptides, camalexin, and 4-OH-ICN, as well as pathogenesis-related proteins. Moreover, genes involved in cell wall and cuticle biosynthesis are constitutively down-regulated in ccc1 mutants, and the cell walls of these mutants exhibit major changes in monosaccharide composition. The role of CCC1 ion transporter activity in the regulation of plant immunity is corroborated by experiments using the specific NKCC inhibitor bumetanide. These results reveal a function for ion transporters in immunity-related cell wall fortification and antimicrobial biosynthesis.
Asunto(s)
Proteínas de Arabidopsis/metabolismo , Arabidopsis/inmunología , Resistencia a la Enfermedad/genética , Pseudomonas syringae/inmunología , Miembro 2 de la Familia de Transportadores de Soluto 12/genética , Arabidopsis/efectos de los fármacos , Arabidopsis/genética , Arabidopsis/microbiología , Proteínas de Arabidopsis/genética , Bumetanida/farmacología , Membrana Celular/genética , Membrana Celular/metabolismo , Membrana Celular/fisiología , Pared Celular/química , Pared Celular/genética , Pared Celular/metabolismo , Resistencia a la Enfermedad/inmunología , Perfilación de la Expresión Génica , Indoles/metabolismo , Monosacáridos/química , Monosacáridos/metabolismo , Mutación , Moléculas de Patrón Molecular Asociado a Patógenos/metabolismo , Enfermedades de las Plantas/genética , Enfermedades de las Plantas/inmunología , Enfermedades de las Plantas/microbiología , Inmunidad de la Planta/efectos de los fármacos , Inmunidad de la Planta/genética , Hojas de la Planta/efectos de los fármacos , Hojas de la Planta/genética , Hojas de la Planta/inmunología , Hojas de la Planta/microbiología , Plantas Modificadas Genéticamente/metabolismo , Pseudomonas syringae/efectos de los fármacos , Pseudomonas syringae/patogenicidad , RNA-Seq , Inhibidores del Simportador de Cloruro Sódico y Cloruro Potásico/farmacología , Simportadores de Cloruro de Sodio-Potasio/metabolismo , Miembro 2 de la Familia de Transportadores de Soluto 12/inmunología , Miembro 2 de la Familia de Transportadores de Soluto 12/metabolismo , Tiazoles/metabolismoRESUMEN
Epidemiological and experimental studies suggest that maternal immune activation (MIA) leads to developmental brain disorders, but whether the pathogenic mechanism impacts neurons already at birth is not known. We now report that MIA abolishes in mice the oxytocin-mediated delivery γ-aminobutyric acid (GABA) shift from depolarizing to hyperpolarizing in CA3 pyramidal neurons, and this is restored by the NKCC1 chloride importer antagonist bumetanide. Furthermore, MIA hippocampal pyramidal neurons at birth have a more exuberant apical arbor organization and increased apical dendritic length than age-matched controls. The frequency of spontaneous glutamatergic postsynaptic currents is also increased in MIA offspring, as well as the pairwise correlation of the synchronized firing of active cells in CA3. These alterations produced by MIA persist, since at P14-15 GABA action remains depolarizing, produces excitatory action, and network activity remains elevated with a higher frequency of spontaneous glutamatergic postsynaptic currents. Therefore, the pathogenic actions of MIA lead to important morphophysiological and network alterations in the hippocampus already at birth.
