Loss of the vacuolar cation channel, AtTPC1, does not impair Ca2+ signals induced by abiotic and biotic stresses

• DOI: 10.1111/j.1365-313x.2007.03342.x
• Publication Date: 2007-11-20T04:04:53Z
• Authors: Stefanie Ranf; Petra Wünnenberg; Justin Lee; Dirk Becker; Marcel Dunkel; Rainer Hedrich; Dierk Scheel; Petra Dietrich
• Keywords: Wild type

The putative two-pore Ca(2+) channel TPC1 has been suggested to be involved in responses abiotic and biotic stresses. We show that AtTPC1 co-localizes with the K(+)-selective AtTPK1 vacuolar membrane. Loss of abolished Ca(2+)-activated slow (SV) currents, which were increased AtTPC1-over-expressing Arabidopsis compared wild-type. A Ca(2+)-insensitive cation channel, as yet uncharacterized, could resolved tpc1-2 knockout plants. kinetics ABA- CO(2)-induced stomatal closure similar wild-type plants, excluding a role SV channels guard-cell signalling response these physiological stimuli. ABA-, K(+)-, Ca(2+)-dependent root growth phenotypes not changed Given permeability mono- divalent cations, question arises whether vivo represents pathway for entry into cytosol. measured aequorin-expressing wild-type, TPC1-over-expressing plants disprove contribution any stimulus-induced signals tested, including stresses (cold, hyperosmotic, salt oxidative), elevation extracellular concentration factors (elf18, flg22). In good agreement, stimulus- gene activation was affected by alterations expression. Together our finding loss did change activity hyperpolarization-activated Ca(2+)-permeable plasma membrane, we conclude TPC1, under conditions, functions without major impact on cytosolic homeostasis.