Research Article: An Extracellular Subtilase Switch for Immune Priming in Arabidopsis

Date Published: June 20, 2013

Publisher: Public Library of Science

Author(s): Vicente Ramírez, Ana López, Brigitte Mauch-Mani, Ma José Gil, Pablo Vera, Jin-Rong Xu.


In higher eukaryotes, induced resistance associates with acquisition of a priming state of the cells for a more effective activation of innate immunity; however, the nature of the components for mounting this type of immunological memory is not well known. We identified an extracellular subtilase from Arabidopsis, SBT3.3, the overexpression of which enhances innate immune responses while the loss of function compromises them. SBT3.3 expression initiates a durable autoinduction mechanism that promotes chromatin remodeling and activates a salicylic acid(SA)-dependent mechanism of priming of defense genes for amplified response. Moreover, SBT3.3 expression-sensitized plants for enhanced expression of the OXI1 kinase gene and activation of MAP kinases following pathogen attack, providing additional clues for the regulation of immune priming by SBT3.3. Conversely, in sbt3.3 mutant plants pathogen-mediated induction of SA-related defense gene expression is drastically reduced and activation of MAP kinases inhibited. Moreover, chromatin remodeling of defense-related genes normally associated with activation of an immune priming response appear inhibited in sbt3.3 plants, further indicating the importance of the extracellular SBT3.3 subtilase in the establishment of immune priming. Our results also point to an epigenetic control in the regulation of plant immunity, since SBT3.3 is up-regulated and priming activated when epigenetic control is impeded. SBT3.3 represents a new regulator of primed immunity.

Partial Text

Plants are continuously faced with threats from pathogenic microorganisms. They counteract microbial infections via activation of an innate immune system in a timely, accurate, and effective manner following pathogen recognition. The innate immune response is thought to act naïvely to individual pathogen encounters and is dependent on the recognition of broadly conserved molecular features, known as microbe-associated molecular patterns (MAMPs), by plasma membrane proteins known as pattern recognition receptors (PRRs). PRR perception of MAMPs at the cell surface leads to a pattern-triggered immune response called PTI [1]. PTI is characterized by the rapid generation of ion fluxes, production of reactive oxygen species (ROS), phosphorylation cascades, and a transcriptional reprograming that favors defense responses over routine cellular requirements [2]. The defense programme is ultimately controlled through the build-up of specific signalling hormone blends, of which salicylic acid (SA) and jasmonic acid (JA) are particularly important, and eventually establish a broad systemic alert state throughout the plant.

Priming, an evolutionarily conserved phenomenon where cells respond to much lower levels of a pathogenic stimulus in a more rapid and robust manner, is an important component of the various forms of IR described in mammals [8]–[10], plants [6], [18] and invertebrates [11]. Despite the importance of priming, the signal component(s) mediating this sensitized state remain elusive. The sensitized state is in part explained by presumably dormant or silent component characters, which accumulate during priming, and are required only after pathogenic challenge [18]. In this respect, pre-stress deposition of two MPK family members of signaling enzymes, MPK3 and MPK6, has been described to play an important role for priming in Arabidopsis [12]. However, it remains undetermined whether or not activation of additional factors operating upstream of the two MPKs is required to establish priming.




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