ABA Regulation of Plant Responses to Drought and Salt Stresses - Abscisic Acid: Metabolism, Transport and Signaling - page 315

16.5 ABA and Maintenance of Ion Homeostasis Under
Drought and Salt Stresses
High salinity stress usually causes osmotic stress when ions accumulate in the
space outside plant cells, whereas it may cause ionic stress when ions concentrate
inside plant cells (Galvan-Ampudia and Testerink 2011 ). Plants suffer ionic stress
not only from the toxic effects of the high cytosolic Na + concentration but also
from the disrupted K + homeostasis resulting from Na + competing for K + bind-
ing sites, which leads to a high Na + /K + ratio. Maintenance of ionic homeosta-
sis by plants is particularly important for adaptation and survival under salt stress
conditions. Hence, plant cells must initiate ion transport systems to maintain ion
homeostasis and avoid ion toxicity. The maintenance of ionic homeostasis during
drought stress is equally as important as that in salt stress, and ABA participates in
regulating ion transporters/channels responding to both high salinity and drought.
The most well-known family involved in ion transport is the NHX family,
which belongs to the monovalent cation-proton antiporter superfamily (Chanroj
et al. 2012 ; Manohar et al. 2011 ; Sze et al. 2004 ). Among NHX family mem-
bers, the salt overly sensitive (SOS) pathway has been intensively studied. The
salt overly sensitive1 (SOS1)/NHX7, a Na + /H + antiporter, was identified by
screening Arabidopsis salt-sensitive mutants (Wu et al. 1996 ). SOS1 is local-
ized at the plasma membrane, and its transcript level is up-regulated by salt
stress but not by ABA (Oh et al. 2010 ). SOS1 is responsible for Na + extrusion
from the cytosol to the extracellular space to maintain the intracellular Na +
concentration at an appropriate level under high salinity stress (Shi et al. 2002 ;
Wu et al. 1996 ). SOS1 requires SOS2 and SOS3 to facilitate proper function.
SOS2 encodes a SnRK3 protein kinase with an N-terminal catalytic domain
and a C-terminal regulatory domain, which phosphorylates the serine residue
(S1138) in the C-terminal domain of SOS1 localized in the cytosol (Liu et al.
2000 ). SOS3, a calcium sensor, encodes a myristoylated calcium-binding protein
that senses cytosolic Ca 2 + . Under high salinity stress, high Na + induces SOS3
binding to cytoplasmic Ca 2 + , facilitates the formation of the SOS3-SOS2 com-
plex, and recruits SOS2 to the plasma membrane to phosphorylate and activate
SOS1. The activated SOS1 promotes Na + efflux to reduce the cytosolic Na +
concentration and mitigate the toxic effects of high salinity (Qiu et al. 2002 ;
Quintero et al. 2011 ; Zhu 2003 ). In addition, the MAP kinase MPK6, CBL10,
SOS3-like SCaBP8, and GIGANTEA (GI) play roles in the SOS pathway. NaCl-
induced phosphatidic acid accumulation activates MPK6, which phosphoryl-
ates the C-terminal of SOS1, and the activated SOS1 responds to the salt stress
(Yu et al. 2010 ). CBL10 interacts with SOS2 and further regulates the activation
of SOS1. GI is reported to be involved in the SOS pathway, as its degradation
releases SOS2 to activate SOS1 under salt stress (Kim et al. 2013 ). SOS1 func-
tions especially at epidermal tissues, and SOS1 mRNA accumulation in salt-tol-
erant T. salsuginea is higher than that in Arabidopsis (Dinneny et al. 2008 ; Oh
et al. 2009 ). In addition, other NHX family members, for instance, NHX5 and