CS-10-5 - Tonoplast-Localized Calcium-ATPases Modulate Ca2+ Signals During Innate Immunity
Sunday, July 15
4:38 PM - 4:58 PM
One of the major hallmarks of early pattern-triggered immunity (PTI) is a rapid influx of Ca2+ into the cytosol within minutes of pathogen-associated molecular pattern (PAMP) recognition. Changes in cytosolic Ca2+ are recognized as ubiquitous elements of cellular signaling networks and are thought to encode stimulus-specific information within their duration, amplitude and frequency; their so-called ‘calcium signature’. Although there is a wealth of observations showing that the PAMP flg22 triggers Ca2+ transients there remains little data defining the elements controlling cellular Ca2+ dynamics that underlie their role in defense signaling activities. Ca2+ signatures are shaped by an interplay between Ca2+ permeable channels that regulate influx and the Ca2+ efflux machinery (e.g. autoinhibited calcium ATPases (ACAs) and cation/H+ antiporters (CAXs)). The work herein focuses on the role played by ACAs, specifically those localized to the tonoplast, within the context of immune responses and how these ACAs regulate Ca2+ transients triggered by the PAMP flg22. Mutant Arabidopsis thaliana plants, aca4/11, with both tonoplast-localized ACAs knocked out were previously shown exhibit spontaneous hypersensitive lesion formation and an increased resistance to the hemibiotrophic bacterial pathogen Pseudomonas syringae. We have recently observed that aca4/11 plants also exhibit calcium transients of higher amplitude compared to wildtype when treated with flg22. Furthermore, an ACA normally localized to the plasma membrane, ACA8, rescues the aca4/11 lesion phenotype when targeted to the tonoplast, further suggesting that regulation of Ca2+ efflux at the tonoplast is an integral component in innate immune signaling.
Simon Gilroy – University of Wisconsin - Madison