Summary I. INTRODUCTION 358 II. GENETIC ANALYSIS OF ABA RESPONSES 359 1. Seed development 359 (a) Maturation 359 (b) Dormancy and germination 361 2. Vegetative responses 365 (a) Root growth 366 (b) Overlapping stress response pathways 367 III. ‘REVERSE GENETIC’ ANALYSIS OF ABA‐REGULATED GENE EXPRESSION 371 1. ABA‐regulated gene products 371 2. Cis‐acting elements 372 3. Trans‐acting factors 375 IV. BIOCHEMICAL AND CELLULAR ANALYSES OF ABA SIGNALLING 378 1. Secondary messengers 379 2. Biochemical approaches to ABA signalling mechanisms 381 (a) Biochemistry of protein kinases and phosphatases 381 (b) Protein‐protein interactions with VP1/ABI3 383 3. ABA receptors 384 4. Cell biology 385 V. CONCLUSIONS AND PERSPECTIVES 387 Acknowledgements 387 References 387 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.