Salinity-induced alteration in expression of ion transporter
genes
In the present study, Pongamia exhibited tissue specific expression of
salt-responsive transporter genes including SOS1, NHXs,
PM-H+-ATPases, V-H+-ATPases, CNGCs,
and other transporter genes. The expression patterns of SOS1 and
SOS1-like genes correlated with Na+ fluoresence
andNa+ion content,indicating that SOS1 genes are
responsible for low Na+ levels in the leaves of
Pongamia by increasing Na+ loading into the xylem/
apoplastic region. Further, the expression levels of SOS1 and SOS1-like
genes increased significantly in salt-treated roots, which may
contribute to apoplastic Na+ depostion under high
salinity. The differential expression of SOS2 and SOS3in the both leaves
and roots suggest their crucial role in salt tolerance of Pongamia
through SOS pathway (Marriboina et al., 2017). In this study, we
observed that the expression of NHX1 was unchaged upon 300 mM salt
stress in both leaves and roots of Pongamia, while there was significant
induction in 500 mM NaCl stress in both leaves and roots, which
correlates with the low levels of Na+ fluoresence
intensity and Na+content data in leaves of 300 mM NaCl
treated plants. At high salt concentration (500 mM NaCl), Pongmia might
induce NHX1 experssion to sequester Na+ ions rapidly
into the vacuole to mitigate the Na+ toxicity.
Similarly, in roots, induced NHX1 expression may indicate the vacuolar
Na+ sequestration. In contrast, NHX1 levels
wereunaffected at intial impostion of stress, suggesting involvement of
other NHXs isofoms for vacuolar Na+ sequestration at
intial stages of salt stress. The differential expresssion of other NHXs
isoforms such as NHX3, NHX6 nd NHX6-like in both leaves and roots
suggests their possible roles in ion homeostasis, plant growth and
development under salt stress (Bassil et al., 2018; Dragwidge et al.,
2018).
In this study,expression of HKT1:1 followed similar trend in both leaves
and roots of salt stressed plants. Previous studies suggested that HKT
family transporter proteins can mediate exclusion of
Na+from leaves and roots by translocating
shoot-to-rootand root-to-shoot Na+ delivery by
withdrwaing Na+ from xylem stream into phloem (Munns
et al., 2012; Hill et al., 2013; An et al., 2017; Zhang et al., 2018).
Induction of HKT1:1 expression upon initial imposition of salt stress in
both leaves and roots may promote Na+ exclusion
tolimit Na+ toxcity in the respective tissues(Zhang et
al., 2018). However, with increasing salt stress treatment time, the
marginal expression of HKT1:1genemay regulate the retrevial of
Na+ from the xylem (Davenport et al., 2007; Ali et
al., 2016). The expression levels of CLC1 indicates that CLC1 may not be
involved in the Cl- vacuolar sequestation (Wei et al.,
2016).
PM-H+-ATPase family pumps playa crucial role in
improving the salt tolerance by maintaing the intracellular pH balance,
transmembrane potential and ion homeostasis under salt stress conditions
(Olfatmiri et al., 2014;Falhof et al., 2016; Shabala et al., 2016). The
diffrences in the expression levels of PM-H+-ATPase
isoforms could be due toconfigurational and/or post-translational
modifications of these isforms under salt stress, which could promote
growth under salinity stress. The increased expression of
V-H+-PPase and V-H+-ATPaseB and E
subunit in leaves of salt treated plants may control the depolarization
of vacuolar membrane potential, which is generated by excess depostion
of Na+ ions in leaves of Pongamia upon prolonged salt
exposure (Graus et al., 2018; Marriboina & Attipalli, 2020a).
An increased expression levels of V-CHX1 may involve in plant growth by
improving cellular ion homeostasis, pH balance and osmoregulation under
saline conditions (Guan et al., 2014; Qi et al., 2014; Liu et al.,
2017). Enhanced experssion of CCX1 may involved in regulation of
intracellular Ca2+ levels, which may help in vacuolar
Na+ sequestration, ROS and ion homeostasis under salt
stress (Yong et al., 2014; Li et al., 2016; Corso et al., 2018).
Differential expression of CNGC5, CNGC17 and CNGC17-like may induce
Ca2+ derived reponses to mitigate the negative effects
of salt stress (Wang et al., 2013; Saand et al., 2015).