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Abstract
Changes in cytosolic free calcium concentration ([Ca2+]cyt) in response to mannitol
(drought) and salt treatments were detected in vivo in intact whole Arabidopsis seedlings.
Transient elevations of [Ca2+]cyt to around 1.5 microM were observed, and these were
substantially inhibited by pretreatment with the calcium-channel blocker lanthanum
and to a lesser extent, the calcium-chelator EGTA. The expression of three genes,
p5cs, which encodes delta(1)-pyrroline-5-carboxylate synthetase (P5CS), the first
enzyme of the proline biosynthesis pathway, rab18 and Iti78 which both encode proteins
of unknown function, was induced by mannitol and salt treatments. The induction of
all three genes by mannitol was inhibited by pretreatment with lanthanum. Salt-induced
p5cs, but not rab18 and Iti78, expression was also inhibited by lanthanum. Induction
of p5cs by mannitol was also inhibited by the calcium channel-blockers gadolinium
and verapamil and the calcium chelator EGTA, further suggesting the involvement of
calcium signalling in this response. Mannitol induced greater levels of p5cs gene
expression than an isoosmolar concentration of salt, at both relatively high and low
concentrations. However, calcium transients were of a similar magnitude and duration
in response to both mannitol and isoosmolar concentrations of salt, suggesting that
a factor other than calcium is involved in the discrimination between drought and
salinity signals in Arabidopsis. In order to gauge the involvement of the vacuole
as an intracellular calcium store in the response of Arabidopsis to mannitol, [Ca2+]cyt
was measured at the microdomain adjacent to the vacuolar membrane. The results obtained
were consistent with a significant calcium release from the vacuole contributing to
the overall mannitol-induced [Ca2+]cyt response. Data obtained by using inhibitors
of inositol signalling suggested that this release was occurring through IP3-dependent
calcium channels.