MECHANISMS TO SALT STRESS: PHYSIOLOGICAL AND MOLECULAR ASPECTS - Salt Marshes - page 139

Gene symbol Donor Acceptor Gene function Elevated character Reference

Pumping H+ from the
cytoplasm into vacuoles to
form the pH gradient

More vigorous growth in
the presence of 200 mM
NaCl

H+-pyrophosphatase
(PPase) gene AVP1

Pasapula et al.
(2011)

A. thaliana Cotton

Na+/H+ antiporters in
plasma membrane,
exchange Na+ or Li+ for
H+

Plasma membrane
Na+/H+ antiporter
SOS1

Accumulating less Na+ in
the xylem transpirational
stream and in the shoot

A. thaliana A. thaliana Shi et al. (2002)

Na+/H+ antiporters in
plasma membrane,
exchange Na+ or Li+ for
H+

Plasma membrane
Na+/H+ antiporter
sodium2 (SOD2)

Accumulating less Na+
and more K+ in the
symplast

Yeast A. thaliana Gao et al. (2003)

Na+/H+ antiporters in
plasma membrane,
exchange Na+ or Li+ for
H+

Plasma membrane
Na+/H+ antiporter SOS A. thaliana A. thaliana

Increased salt tolerance Yang et al. (2009)

Na+/H+ antiporters in
plasma membrane,
exchange Na+ or Li+ for
H+

Active loading of Na+
into the xylem, and Na+
and K+ compart-
mentalization

Plasma membrane
Na+/H+ antiporter
SISOS

Huertas et al.
(2012)

Tomato Tomato

Na+/H+ antiporters in
plasma membrane,
exchange Na+ or Li+ for
H+

Superior growth and
accumulated less Na+
and more K+ in roots after
350 mM NaCl treatment

Plasma membrane
Na+/H+ antiporter
SOS1, SOS2, SOS3

A. thaliana Tall fescue Ma et al. (2013)

Salinity exposure triggers complicated signaling events, so the way in which the stresses
are sensed and transported by salt -stress signaling provides us with a clue to understand the
regulation mechanisms of plants. The SOS signaling pathway is elucidated at the earliest and
it consists of three key components: SOS3, SOS2 and SOS1. SOS3 is a Ca 2+ sensor (Liu and
Zhu 1998). SOS2 is a serine/threonine protein kinase (Liu et al. 2000). The SOS3 can sense
the perturbation of Ca 2+ levels in cytoplast caused by salt stress and then bind to the SOS2.
Then the SOS3/SOS2 complex phosphorylates and activates SOS1, hence the activated SOS1
has the ability to export excess ions and contribute to Na + ion homeostasis (Liu et al. 2000;
Liu and Zhu 1998; Quintero et al. 2002). SOS1 was discovered to be the downstream target of
MPK6 by GST-pull-down assay (Smékalová et al. 2013). Moreover, during salt stress the
phosphorylation degree of SOS1 increases (Davies et al. 2005). There are many other
researches attesting that the components of the signaling pathway may be regulated by salt
stress directly or have a hand in other signaling pathways of the stress to affect responses
indirectly (Shabala et al. 2005; Mahajan and Tuteja 2005; Qiu et al. 2002).
The NHXs are the vacuolar Na + /H + antiporters. In a review published recently, NHXs
were demonstrated to play roles in cell expansion, cell volume regulation, ion homeostasis,
osmotic adjustment, pH regulation, protein processing and so on (Rengasamy 2010). In
genetic engineering, the hypersensitive phenotype of sos1 demonstrated powerfully the key
position of SOS signaling pathway in salt-stress. Compared to control leaves, the H + -ATPase
in tonoplast vesicles increased two-fold in salt-treated leaves (Qiu et al. 2007).
Overexpression of NHX may reduce cytosolic Na + concentration and improve salt tolerance
by efficient sequestration (Apse et al. 1999). Its overexpression confers salt tolerance to a
wide range of plants (Yang et al. 2009). In Table 1, transgenic plants for different ion
transporters with enhanced ion homeostasis are listed for reference.
In addition, the HKT family also plays vital functions in maintaining ions homeostasis.
The HKT proteins act as Na + /K + symporters and Na + -selective transporters, involved in