Publication Date:
2020-07-20
Description:
One of the major events of early plant immune responses is a rapid influx of Ca2+into the cytosol following pathogen recognition. Indeed, changes in cytosolic Ca2+are recognized as ubiquitous elements of cellular signaling networks and are thought to encode stimulus-specific information in their duration, amplitude, and frequency. Despite the wealth of observations showing that the bacterial elicitor peptide flg22 triggers Ca2+transients, there remain limited data defining the molecular identities of Ca2+transporters involved in shaping the cellular Ca2+dynamics during the triggering of the defense response network. However, the autoinhibited Ca2+-ATPase (ACA) pumps that act to expel Ca2+from the cytosol have been linked to these events, with knockouts in the vacuolar members of this family showing hypersensitive lesion-mimic phenotypes. We have therefore explored how the two tonoplast-localized pumps, ACA4 and ACA11, impact flg22-dependent Ca2+signaling and related defense responses. The double-knockoutaca4/11exhibited increased basal Ca2+levels and Ca2+signals of higher amplitude than wild-type plants. Both the aberrant Ca2+dynamics and associated defense-related phenotypes could be suppressed by growing theaca4/11seedlings at elevated temperatures. Relocalization of ACA8 from its normal cellular locale of the plasma membrane to the tonoplast also suppressed theaca4/11phenotypes but not when a catalytically inactive mutant was used. These observations indicate that regulation of vacuolar Ca2+sequestration is an integral component of plant immune signaling, but also that the action of tonoplast-localized Ca2+pumps does not require specific regulatory elements not found in plasma membrane-localized pumps.
Print ISSN:
0027-8424
Electronic ISSN:
1091-6490
Topics:
Biology
,
Medicine
,
Natural Sciences in General
