Disease relevance of ABA1

• ABA2 protein, produced in Escherichia coli, exhibits in vitro zeaxanthin epoxidase activity [1].
• Double mutant analysis of hos5-1 and the ABA-deficient aba1-1 as well as the ABA-insensitive abi1-1 mutant indicated that the osmotic stress hypersensitivity of hos5-1 is not affected by ABA deficiency or insensitivity [2].
• In an attempt to elucidate the physiological role of ABA in seed dormancy and the adaptive response to dehydration, we isolated an ABA-deficient mutant of Arabidopsis thaliana (L.) Heynh. which germinated in the presence of a gibberellin biosynthetic inhibitor [3].

High impact information on ABA1

• Consistent with this result, we show that three ABA-deficient mutants (aba1-1, aba2-1, and aba3-2) are also glucose insensitive [4].
• Molecular identification of zeaxanthin epoxidase of Nicotiana plumbaginifolia, a gene involved in abscisic acid biosynthesis and corresponding to the ABA locus of Arabidopsis thaliana [1].
• Mutant ibs3 is affected in the regulation of the ABA1 gene encoding the abscisic acid (ABA) biosynthetic enzyme zeaxanthin epoxidase [5].
• By contrast, ibs2 and ibs3 showed reduced BABA-induced tolerance to salt, which correlated with an affected priming for ABA-inducible gene expression [5].
• Whereas ibs1 was reduced in priming for salicylate (SA)-dependent trailing necrosis, mutants ibs2 and ibs3 were affected in the priming for callose deposition [5].

Biological context of ABA1

• Regulation of osmotic stress-responsive gene expression by the LOS6/ABA1 locus in Arabidopsis [6].
• Here we report the isolation, characterization, and cloning of a mutation, los6, which diminished osmotic stress activation of a reporter gene [6].
• By contrast, ABA deficiency as conditioned by the mutations in the ABA1 and ABA2 genes, which encode enzymes involved in ABA biosynthesis, resulted in upregulation of basal and induced transcription from JA-ethylene responsive defense genes [7].
• The high levels of zeaxanthin in npq2 affected the kinetics of induction and relaxation but not the extent of nonphotochemical quenching [8].
• ABA-deficient mutants, however, display a stunted phenotype even under well-watered conditions and high relative humidity, which suggests that growth promotion may also be one of the roles of endogenous ABA [9].

Anatomical context of ABA1

• Experiments on purified thylakoid membranes from all three mutants showed that the major source of the difference between the npq2 and wild-type preparations was a change in pigment to protein interactions, which can explain the lower chlorophyll fluorescence yield in the npq2 samples [10].

Associations of ABA1 with chemical compounds

• Furthermore, we found that there exists a positive feedback regulation by ABA on the expression of LOS6/ABA1, which may underscore a quick adaptation strategy for plants under osmotic stress [6].
• Natural variability was found in the induction by NaCl and ABA of NCED3 and ABA1 expression in different Arabidopsis accessions, although NCED3 expression was clearly predominant [11].
• Mutations in nicotinamide adenine dinucleotide phosphate oxidase homolog genes (atrbohB and D), ABA biosynthesis mutants (aba1, aba2, and aba3), and NahG transgenic lines (salicylic acid deficient) showed weaker defects [12].
• A third mutant, aba1, accumulates normal levels of lutein and substitutes zeaxanthin for violaxanthin and neoxanthin [13].
• Sequence analyses of both violaxanthin de-epoxidase and zeaxanthin epoxidase establish the xanthophyll cycle enzymes as members of the lipocalin family of proteins [14].

Other interactions of ABA1

• Both abscisic acid (ABA)-dependent and ABA-independent pathways govern the induction of NCED3, AAO3 and ABA1 in response to salt stress [11].
• Furthermore, ABA-plus-mannitol treatments were additive towards COR47 gene expression; however, the ABA-deficient aba1 mutant showed reduced COR expression relative to the wild type in response to mannitol and ABA-plus-mannitol treatments [15].
• Use of abi1-1 (ABA-insensitive) and aba1-1 (ABA-deficient) Arabidopsis mutants indicated that drought induction of AtLEA5 required ABA synthesis but was independent of the ABI1 gene product [16].
• The induction of ATHB-7 was shown to be mediated strictly via ABA, since no induction of ATHB-7 was detectable in the ABA-deficient mutant aba-3 subjected to drought treatment [17].
• Induction of AtP5CS1 mRNA accumulation in salt-treated seedlings involves an immediate early transcriptional response regulated by ABA signalling that is not inhibited by cycloheximide, but abolished by the deficiency of ABA biosynthesis in the aba1 Arabidopsis mutant [18].

Analytical, diagnostic and therapeutic context of ABA1

• Complementation tests with different ABA-deficient mutants indicated that sre2-1 and sre2-2 mutants were allelic to aao3-1, and therefore they were renamed as aao3-2 and aao3-3, respectively [19].
• An ABA immunoassay supported this hypothesis: ABA-entrained plants showed a transient increase in endogenous ABA level from 220 to 250 pmol g-1 fresh mass at 1-2 h of the training period, whereas ABA-deficient (aba2) mutants did not [20].

References