The Arabidopsis cax3 mutants display altered salt tolerance, pH sensitivity and reduced plasma membrane H+-ATPase activity

Abstract

Perturbing CAX1, an Arabidopsis vacuolar H+/Ca2+ antiporter, and the related vacuolar transporter CAX3, has been previously shown to cause severe growth defects; however, the specific function of CAX3 has remained elusive. Here, we describe plant phenotypes that are shared among cax1 and cax3 including an increased sensitivity to both abscisic acid (ABA) and sugar during germination, and an increased tolerance to ethylene during early seedling development. We have also identified phenotypes unique to cax3, namely salt, lithium and low pH sensitivity. We used biochemical measurements to ascribe these cax3 sensitivities to a reduction in vacuolar H+/Ca2+ transport during salt stress and decreased plasma membrane H+-ATPase activity. These findings catalog an array of CAX phenotypes and assign a specific role for CAX3 in response to salt tolerance.

CAX‐ing a wide net: Cation/H+ transporters in metal remediation and abiotic stress signalling

“…2005), and evidence suggests altered regulation of proton pumps when CAX expression is deregulated (Zhao et al . 2008; Conn et al . 2011).…”

Sodium as nutrient and toxicant

“…Non-selective cation channels (NSCCs) can also mediate Na + fluxes (Zhao et al 2011), although their molecular/genetic characterization is currently unknown. At the tonoplast, Na + sequestration is linked to cation exchangers (CAX and NHX; Zhao et al 2008;Apse et al 2003) and vacuolar channels (SV and FV;Ivashikina and Hedrich 2005;Isayenkov et al 2010). SV channels are also blocked by luminal Na + (Ivashikina and Hedrich 2005).…”

“…At the tonoplast, vacuolar sequestration of Na + has been attributed to the function of Na + /H + exchangers (NHX; Blumwald and Poole 1985;Apse et al 1999Apse et al , 2003 and both slow-vacuolar (SV) (Hedrich and Neher 1987;Schönknecht et al 2002;Ivashikina and Hedrich 2005) and fast-vacuolar (FV) channels (Isayenkov et al 2010). It has further been suggested that members of the cation exchanger (CAX) family could transport Na + (Luo et al 2005; see also Zhao et al 2008), but, again, none of these candidates is a part of current models of guard cell function. No leading reviews or textbook treatises on stomatal guard cell function have incorporated these flexibilities and, instead, they make the case for very specific, and central, engagement of K + channels/transporters as integrated into a tightly orchestrated cascade of events, involving hormone binding, Ca 2+ fluxes, and membrane potential activation of K + fluxes (Schroeder et al 2001).…”

Vacuolar Ca2+/H+ Transport Activity Is Required for Systemic Phosphate Homeostasis Involving Shoot-to-Root Signaling in Arabidopsis

“…However, only CAX1 to CAX4 have been functionally characterized to possess a vacuolar Ca 2+ /H + exchange activity. Whereas CAX1 and CAX3 mediated specifically Ca 2+ transport (Hirschi, 1999;Catala et al, 2003;Cheng et al, 2003;Mei et al, 2007;Zhao et al, 2008), CAX2 and CAX4 were documented to have high transport and selectivity for cadmium ions (Cd 2+ ) over Ca 2+ in tonoplast vesicles (Hirschi et al, 2000;Cheng et al, 2002;Pittman et al, 2004;Koren'kov et al, 2007).…”

“…Conversely, transgenic tobacco plants overexpressing CAX1 were hypersensitive to ion imbalance and cold shock and exhibited Ca 2+ -deficient symptoms in spite of increased accumulation of Ca 2+ (Hirschi, 1999). Loss-offunction of CAX3, a close homolog of CAX1, increased the sensitivity to salt stress, lithium, and low pH (Zhao et al, 2008). While cax1 and cax3 single mutants displayed subtle phenotypes, the cax1/cax3 double mutant showed stunted growth with chlorosis on the leaf tips and a drastic reduction in silique size and seed numbers (Cheng et al, 2005).…”