4.3 PTOX and NDH-mediated cyclic electron transfer
Under stress conditions, the cyclic electron transfer rate usually
increases (Brayton et al., 2006; Shikanai 2007; Takahashi et al., 2013;
Strend et al., 2015). In contrast, here we show that in SA , which
has a great capacity of channeling electrons to PTOX, the rate of cyclic
electron transfer rate decreased (Figure 6). This is clearly shown by
data from the post-illumination Fo rise (PIR) signal, which was used
here to assay NDH (Burrows et al., 1998). Using this method, we found a
stark contrast in the responses of NDH-dependent CEF and PTOX to salt
stress between species (SA and SV ). In SV , the
strong stimulation of NDH-dependent CEF following salt stress (236%)
was concurrent to a nearly stable PTOX level (Figs. 6 and 8). However,
in SA , we observed a decline in the NDH-dependent CEF (Figure 6)
together with an increase of PTOX expression levels, which was
up-regulated by up to 4 times compared to the control as assessed by
both RNA-expression abundance and protein abundance (Figure 8).
Our finding of this negative relationship between PTOX and NDH-CEF is in
line with a number of earlier reports, e.g. Ahmad et al. (2012)
demonstrated a dramatic decline in NDH activity in tobacco expressing
PTOX from green algae (Cr-PTOX1); PTOX competes efficiently with CEF for
plastoquinol (PQH2) in the CRTI-expressing (carotene desaturase) lines
(Galzerano et al., 2014); Joët et al. (2002) also showed a decrease in
NDH-dependent CEF in tobacco transgenic lines expressing PTOX from
Arabidopsis. The activity of cyclic electron transfer is regulated by an
array of mechanisms, including redox status (Lasano et al., 2001;
Breyton et al., 2006; Takahashi et al., 2013),
H2O2 (Strand et al., 2015), metabolite
levels (Livingston et al., 2010), Ca signaling (Terashima et al., 2012;
Lascano et al., 2003), and even phosphorylation of NDH components
(Lascano et al., 2003). It is likely that NaCl induced differential
changes in the NDH and PTOX, though mechanism is complexly unknown. It
is possible that some internal signals from chloroplast, such as redox
status of chloroplast electron transfer chain, or particular compound in
the photosynthetic carbon metabolism, or even
H2O2, might differentially regulate PTOX
and NDH-CET. Mechanisms how PTOX and NDH-CET were differentially
regulated under NaCl needs further elucidation. It is worth mentioning
here that SA has been used as a model halophyte grass species to
study adaptation to plants to salt stress and to mine salt
stress-responsive genes (Subudhi & Baisakh, 2011). Several ealier
studies have demonstrated the utility of genes from this halophyte to
improve crop salt tolerance (Baisakh et al. 2012; Karan & Subudhi,
2012a, b). Therefore, elucidation of how PTOX and NDH-CET respond under
NaCl to protect photosystem and leaf functioning can help develop new
strategy to protect photosystems under salt stress.
Abbreviations : A , photosynthetic rate; CAT,
catalase; CEF, cyclic electron flow; Chl, chlorophyll; DAB, 3, 3’
diaminobenzidine; DBMIB, 2,5-dibromo-3-methyl-6-isopropyl-p-
benzoquinone; ETC, electron transport chain; FI, fluorescence induction;gs , stomatal conductance; Fo, minimum
fluorescence (PSII RCs open); Fm, maximum fluorescence
(PSII RCs close); gETC, conductance of the electron
transfer chain; n -PG, n -propyl gallate (n -PG,
3,4,5-trihydroxy-benzoic acid-n-propyl ester); NBT, nitroblue
tetrazolium; NDH, NAD(P)H dehydrogenase; NPQ, non-photochemical
quenching; PQ, plastoquinone; PQH2, plastoquinol; PTOX,
plastid terminal oxidase; P700, photosystem I reaction
center; ROS, reactive oxygen species; SP, saturating pulse; SOD,
superoxide dismutase; SV , Setaria viridis ; SA ,Spartina alterniflora .