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Salt stress is known to mimic water stress limiting CO
2
inflow by lowering con-
ductance of stomata and mesophyll and by impairing carbon metabolism (Delfine
et al.
1998
,
1999
). Loreto and Delfine (
2000
) tested whether revival from mod-
est salt treatment could result in bursts of isoprene emission and concluded that
the progression leading to isoprene release is resistant than photosynthesis to salt
stress, and that a secondary source of isoprene, independent of photosynthesis, is
induced by salt-stress. In case of short-term drought stress, significant reductions in
photosynthesis were observed, whereas isoprene emission was either not repressed
or became reduced in
Quercus virginiana
(Tingey et al.
1981
) and
Pueraria lo-
bata
(Sharkey and Loreto
1993
). On the other hand, there was a good relationship
between terpene emission and plant water status. The emission of several mono-
terpenes and sesquiterpenes was studied in Mediterranean species (
Rosmarinus of-
ficinalis, Pinus halepensis, Cistus albidus
and
Quercus coccifera
) upon subjecting
them to long term water dehydration stress (Ormeno et al.
2007
). There was a slow
decrease of emissions in plants exposed to long term water deficit periods in
P.
halepensis
and
C. albidus
as compared to decrease in sesquiterpene release of
R.
officinali.
Šimpraga et al. (
2011
) opined that drought stress can affect the VOC
emissions in plants. In their experiments with young Common beech, the authors
observed sudden burst of non-monoterpene class of VOCs during acute drought
stress indicating opportunities for plant sensing using VOCs.
Manipulating the Synthesis of VOCs
Isoprenoids have been demonstrated to confer defense against abiotic stress fac-
tors, mainly thermal stress and oxidative stress conditions. A full understanding
of the function of terpenes in plant defense process will require experiments at the
molecular level, as terpenes may induce the expression of a number of stress-related
genes. Studies in this direction by using inhibitors like fossidomycin that can inhibit
the MEP pathway, fumigating non-isoprene synthesizing plants with exogenous iso-
prenoid compounds and transgenic plants either expressing terpene synthesis genes
or gene silencing, have yielded results supporting their protection against stresses
(Dudareva and Pichersky
2008
; Vickers et al.
2009a
).
The enzymes leading to the production of monoterpene all appear to be active
in the plastids, as all the genes in this pathway possess plastid-targeting signals
(Haudenschild and Croteau
1998
) and seems to be localized in chloroplasts (Bou-
vier et al.
2000
) and leucoplasts (Turner et al.
1999
). The principal functional role
of isoprene emission in plants is associated with the protection of leaf physiological
processes against oxidative stress induced by heat (Sharkey and Yeh
2001
). Behnke
et al. (
2007
) analyzed this 'physiological role' by testing transgenic Grey poplar
plants in which expression of
isoprene synthase
(
ISPS
) was either silenced via RNA
interference (RNAi) mechanism or upregulated by over-expression of the
ISPS
gene. Despite increased
ISPS
mRNA levels, there was no steady increase in isoprene
release in the over-expressing lines, suggesting that
ISPS
could be regulated at the
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