Disease relevance of ABI4

• Although overexpression of ABI5 confers hypersensitivity to ABA and sugar, as previously described for ABI4 and ABI3 overexpression lines, it has relatively limited effects on enhancing ABA-responsive gene expression [1].

High impact information on ABI4

• Thus, ABI4 might be a regulator involved in both glucose- and seed-specific ABA signaling [2].
• These results provide the first direct evidence to support a novel and central role of ABA in plant glucose responses mediated through glucose regulation of both ABA levels by GIN5 and ABA signaling by GIN6/ABI4 [2].
• Analysis of Arabidopsis glucose insensitive mutants, gin5 and gin6, reveals a central role of the plant hormone ABA in the regulation of plant vegetative development by sugar [2].
• Surprisingly, only abi4 and abi5-1 but not other ABA-insensitive signaling mutants (abi1-1, abi2-1, and abi3-1) exhibit glucose insensitivity, indicating the involvement of a distinct ABA signaling pathway in glucose responses [2].
• The cbl9 mutant plants showed enhanced expression of genes involved in ABA signaling, such as ABA-INSENSITIVE 4 and 5 [3].

Biological context of ABI4

• To determine whether ABI4 is necessary and/or sufficient for ABA response, we assayed the effects of loss of ABI4 function and ectopic ABI4 expression on growth and gene expression [4].
• We examined genetic interactions among three ABA response loci, ABI3, ABI4, and ABI5, by comparing phenotypes of mutants, ectopic expression lines, mutants carrying an ectopically expressed transgene, and the corresponding wild-type lines [4].
• Expression analyses showed that despite the seed-specific nature of the mutant phenotype, ABI4 expression is not seed specific [5].
• Identification of the maize ABI4 ortholog and the demonstration of its binding to a known ABA response element provide a link between ABA-mediated kernel development and the regulation of ABA response genes [6].
• The Arabidopsis abscisic acid response locus ABI4 encodes an APETALA 2 domain protein [5].

Associations of ABI4 with chemical compounds

• We also show that ABA INSENSITIVE4 (ABI4) expression is confined to the embryo, accounts for the major differences in embryo response to ABA, and defines a role for ABI4 as a repressor of lipid breakdown [7].
• In addition, NaCl-, KCl-, and mannitol-tolerant as well as abscisic-acid-insensitive germination was displayed by sañ5, whose genetic and molecular characterization indicates that it carries an extremely hypomorphic or null allele of the ABI4 gene, its deduced protein product lacking the APETALA2 DNA binding domain [8].
• Both of these responses were modified by sucrose treatment, indicating that ABI4 has a role in connecting ABA and sugar in regulating Pro accumulation [9].
• ABI4 mediates the effects of exogenous trehalose on Arabidopsis growth and starch breakdown [10].
• Results indicate that the germination inhibition by glucose cannot be antagonized by ethylene or gibberellin and is independent of the HXK1/ABA/ ABI4 signalling cascade [11].
• Analysis of transcript abundance for AOX1a in abi4 mutant lines revealed significantly increased levels of AOX1a mRNA that could not be further induced by rotenone, consistent with the role of ABI4 as a repressor that is derepressed in response to rotenone [12].

Other interactions of ABI4

• These results suggest that PA is involved in ABA signaling and that AtLPP2 functions as a negative regulator upstream of ABI4, which encodes an AP2-type transcription factor, in ABA signaling during germination [13].
• Comparison of expression of eight ABI5-homologous genes shows overlapping regulation by ABI3, ABI4, and ABI5, suggestive of a combinatorial network involving positive and negative regulatory interactions [1].
• Arabidopsis thaliana BAC T07M07 encoding the abscisic acid-insensitive 4 (ABI4) locus has been sequenced completely [14].
• Glc regulation of ABI4 and CTR1 transcripts is dependent on the developmental stage [15].
• Expression analysis by quantitative reverse transcription-PCR in transgenic plants showed up-regulation of the ABI4 and CAB1 genes [16].

References