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deficient 2/isochorismate synthase 1 (SID2/ICS1) gene, which encodes the SA
biosynthetic enzyme, increased under UV-C light irradiation in wild type but not
NahG plants. Although UV-C induced expression of FT and CO in wild type, these
genes were not induced in NahG plants.
The exogenous application of SA at 100 lM accelerated flowering in Col, but
the NahG plants were not responsive to SA treatment. SA also regulates flowering
time in non-stressed plants. SA-deficient NahG plants exhibit late flowering
(Martínez et al. 2004 ). The siz1 mutant with elevated SA level shows an early
flowering phenotype under SD, and this phenotype is suppressed by the expression
of NahG (Jin et al. 2008 ). Exogenous SA treatment reduced the expression of the
flower-inhibiting gene, FLC. Thus, UV-C-induced flowering requires the enhanced
expression of FT and the reduced expression of FLC.
The genome-wide analyses of transcriptomes revealed the down-regulation of
Pathogen and Circadian Controlled 1 (PCC1) in SA-deficient A. thaliana plants
(Segarra et al. 2010 ). PCC1 was initially characterized as a circadian clock-reg-
ulated gene that is rapidly up-regulated after pathogen inoculation. The expression
of PCC1 was strongly activated under UV-C light irradiation in Col but not in
NahG plants. SA application also activated PCC1 expression. The activation of
PCC1 expression required CO. RNAi transgenic plants contained lower levels of
FT transcript. The over-expression of PCC1 did not accelerate flowering, but the
RNAi-mediated suppression of its expression delayed flowering. UV-C light
irradiation of plants accelerates flowering through a SA-dependent process in wild
type but not RNAi transgenic plants with reduced expression of PCC1, suggesting
that neither SA nor PCC1 alone is sufficient to accelerate flowering in A. thaliana.
These results suggest the involvement of SA in UV-C stress-induced flowering
in A. thaliana.
9 Conclusion
It is apparent that plants flower in response to several stress conditions. Con-
stantly exposed to stresses that negatively affect growth and development, plants
establish protection and adaptation strategies to minimize stress influences.
However, protection or adaptation might not be sufficient under severe stress
conditions. Thus, precocious flowering might assist in species preservation under
such conditions. Thus, stress-induced flowering can be considered as the ultimate
adaptation to stress and should be considered a central component, along with
tolerance, resistance and avoidance, of stress physiology. The production of SA,
through the activation of PAL, and the expression of FT have been suggested to
be involved in the regulation of stress-induced flowering in several plant species.
Therefore, an important subject to be studied in the future is the interaction
between SA and FT.
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