Recent progress in ABA signalling is summarized from the perspectives gained by genetic (mutant) analysis, 'reverse genetics' (starting from unknown ABA-inducible sequences and working backwards) and biochemical studies. What emerges is a cell-biological model of overlapping tissue-specific stress (e.g. drought, salt and cold) and developmental (e.g. sugars and other hormones) response pathways that integrate into responses mediated by ABA, including but not limited to seed maturation, dormancy, inhibition of cell division and germination, stomatal closure and changes in gene expression leading to stress adaptation. ABA signalling involves putative ABA receptors (extracellular or intracellular), cell-surface membrane proteins including ion channels, glycoproteins and membrane trafficking components, secondary messengers such as phosphatidic acid, inositol 1,4,5-trisphosphate, cyclic ADP-ribose and calcium, and protein phosphorylation/dephosphorylation cascades leading to chromatin remodelling and binding of transcriptional complexes to ABA-responsive promoter elements. The large gaps in our understanding of complex regulatory networks such as ABA signalling can be best addressed by multidisciplinary, integrated approaches such as those discussed.
- Plasma membrane
- Regulation of gene expression
- Secondary messenger
- Signal trasduction