RESUMO
Transient cytosolic Ca(2+) ([Ca(2+)](cyt)) elevations are early events in plant signaling pathways including those related to abiotic stress. The restoration of [Ca(2+)](cyt) to prestimulus levels involves ATP-driven Ca(2+) pumps, but direct evidence for an essential role of a plant Ca(2+)-ATPase in abiotic stress adaptation is missing. Here, we report on a stress-responsive Ca(2+)-ATPase gene (PCA1) from the moss Physcomitrella patens. Functional analysis of PCA1 in a Ca(2+) transport-deficient yeast mutant suggests that PCA1 encodes a P(IIB)-type Ca(2+)-ATPase harboring an N-terminal autoinhibitory domain. In vivo localizations identified membranes of small vacuoles as the integration site for a PCA1:GFP fusion protein. PCA1 mRNA levels are up-regulated by dehydration, NaCl, and abscisic acid, and PCA1 loss-of-function mutants (DeltaPCA1) exhibit an enhanced susceptibility to salt stress. The DeltaPCA1 lines show sustained elevated [Ca(2+)](cyt) in response to salt treatment in contrast to WT that shows transient Ca(2+) elevations, indicating a direct role for PCA1 in the restoration of prestimulus [Ca(2+)](cyt). The altered Ca(2+) response of the DeltaPCA1 mutant lines correlates with altered expression levels of stress-induced genes, suggesting disturbance of a stress-associated signaling pathway. We propose that PCA1 is an essential component for abiotic stress adaptation in Physcomitrella involved in the generation of a specific salt-induced Ca(2+) signature.
