Physiology and Molecular Biology of Stress ... - KHAM PHA MOI

Freezing Stress
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in cytosolic Ca 2+ when the temperature is lowered to induce cold acclimation (Knight,
2000). However, this phenomenon is not conclusive as it is only demonstrated under a
fast cooling rate and not if the temperature decrease is less than 10ºC in one hour (Plieth
et al., 1999).
Many aspects of plant development, including stress tolerance, are regulated
by antagonistic interactions between plant hormones e.g. abscisic acid (ABA) and
gibberellins (Gomez-Cadenas et al., 2001); auxins and cytokinins (Coenen et al., 2003);
and by synergistic interactions e.g. ABA and jasmonic acid (JA) (Wilen et al., 1994).
Abscisic acid a growth inhibitor, induces cold acclimation in a wide range of plants
(Chen and Gusta 1983, Reaney et al., 1989), whereas gibberellins are growth promoters
and counteract the effect of ABA (Reaney et al., 1989). Recent analysis of Arabidopsis
mutants demonstrated strong interactions between ABA and other signalling pathways,
including auxin, sugar and ethylene (Lu and Fedoroff, 2000, Gazzarrini and
McCourt, 2003). Arabidopsis mutants have been identified that show reduced sensitivity
to both ABA and auxins (Suzuki et al., 2001, Monroe-Augustus et al., 2003).
There is substantial evidence implicating MAPK pathways in both ABA and auxin
signalling.
There is a great deal of confusion regarding the role of ABA in the development
and maintenance of freezing tolerance and this has led to the suggestion that
there are two pathways; an ABA independent pathway and an ABA dependent pathway.
This evidence is based on the finding that ABA at non acclimating temperatures
fails to up regulate several cold associated genes. It has been assumed that all cold
upregulated genes respond similarly, and therefore, genes that do not respond to exogenous
ABA, but only to low temperatures are independent of ABA. Few attempts in
these studies have made the effort to establish the uptake of ABA and its translocation
to the site of interest or if ABA is absorbed by the cells in question. Foliarly applied
ABA is not readily absorbed in contrast to a root drench application. Often ABA
mutants that are either insensitive to ABA or are deficient in ABA are used to determine
the role of ABA in the stress response. In many of these studies using ABA insensitive
mutants the quality of exogenous ABA taken up by the cell in question has not
been determined, or if exogenous ABA has been degraded or sequestered or if nonstress
ABA responsive genes have been upregulated or if the temperature is conducive
to the binding of ABA at its receptor site. ABA deficient mutants have reduced
levels of ABA in comparison to the wild types. The limitation of these mutants of the
optimum concentration for gene regulation is not known and therefore these mutants
are always “leaky”. There are very specific, highly quantitative tests available to measure
ABA (Chiwocha et al., 2001) in contrast to the less specific ELISA tests. In
addition there are at least three unique pathways for the synthesis of ABA (Zhou et al.,
2004). Thus a mutation in one pathway may not necessarily affect another pathway.
Therefore there is an inherent ambiguity in using these mutants to establish the role of
ABA in stress. Other possibilities for lack of response to ABA is degradation, sequestration
and unavailability of ABA binding sites. Often ABA acts in concert with other