Furthermore, some “ABA response regulators” appear to also
function in networks regulating response to sugars, salt, and
most known hormones. Although initially selected on the basis of
increased or decreased ABA response, not all mutants show consistent hyper- or hyposensitivity for all ABA-regulated responses.
Thus it is most useful to consider genetic interactions in the context of specific cell types, since the participants and outcomes of
ABA signaling vary. For example, comparison of ABA-regulated
transcriptomes identify 1-10% of the genome as ABA-regulated
in any given experiment, for a total of nearly 6000 ABA-induced
and a similar number of ABA-repressed genes, but very few of
the induced genes were common to nearly all conditions (Choudhury and Lahiri, 2010; Wang et al., 2011) (Table 3). Over half of
this core set are either signaling factors (ABI-clade PP2Cs, transcription factors, kinases, lipid binding or assorted transporters)
or desiccation protectants of the dehydrin or late embryogenesis
abundant classes. Despite their apparent central nature in ABA
signaling, loss of function for these individual genes has little to
no effect on ABA response, presumably due to redundancy with
other factors. Interestingly, the core set of repressed genes includes multiple members of the PYR/PYL/RCAR receptor family,
providing a mechanism to desensitize ABA response and restore
homeostasis. In the following sections, we will consider the ABA
signaling networks in maturing seeds, germination, seedlings,
vegetative stress responses, stomatal regulation, pathogen response, flowering, and senescence
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