Scientist I University of Wisconsin, Madison Madison, Wisconsin
Body of Abstract: Flooding represents a major threat to global agricultural productivity and food security. Such stresses encountered by plants involve stimulus-specific cellular transport of Ca2+ ions, mediated by an array of channels and pumps, leading to physiological changes. As a result of flooding, plants also experience limited oxygen availability (hypoxia), resulting in altered Ca2+ signaling. However, the biological and molecular roles of pumps regulating this flooding triggered Ca2+ signaling are still relatively unknown.
To help define components of this regulatory network, we therefore mined the publicly available transcriptomes of Arabidopsis plants subjected to flooding or hypoxic stress for rapidly upregulated, Ca2+-related transcripts. Candidates emerging from this study included two Ca2+ transporters, AUTOINHIBITED CA2+ ATPASE 1 (ACA1) and CATION EXCHANGER 2 (CAX2), which are predicted to affect the dynamics of Ca2+ signals most directly associated with flooding/hypoxia stresses and hence, further used them to test their role in regulating flooding-related responses.
Using a combination of physiological, biochemical, and molecular-based assays, current findings revealed that knockout mutants in CAX2 but not ACA1 showed enhanced survival to both short and long-term flooding. In addition, we also discovered that knocking out CAX2 leads to slightly elevated resting Ca2+ levels and larger flooding-induced Ca2+ signals. The elevated basal levels also triggered some flooding-responsive genes to be constitutively activated in the cax2 mutant plants, preadapting them to flooding stress. These effects are consistent with a role for this vacuolar pump, exporting Ca2+ ions from the cytosol whereas, when these pumps are inactive, it attenuates the Ca2+ signals, which in turn, triggers adaptation to flooding. These observations suggest that CAX2 is an important component regulating the activity of the flooding response network, likely through its effects on the flooding-induced Ca2+-signaling network, highlighting the key role of the vacuole in modulating flooding-related signaling systems.