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The genetics of adaptive responses to drought stress: abscisic acid‐dependent and abscisic acid‐independent signalling components
Author(s) -
Riera Marta,
Valon Christiane,
Fenzi Francesca,
Giraudat Jérôme,
Leung Jeffrey
Publication year - 2005
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.2005.00469.x
Subject(s) - abscisic acid , biology , arabidopsis thaliana , gene , arabidopsis , mutant , complementation , signalling , genetics , computational biology , microbiology and biotechnology
Drought stress is the major limitation to crop productivity. However, crops are genetically complex with many loci contributing quantitatively to a given physiological trait. Nonetheless, significant in‐roads into the molecular mechanisms of drought‐adaptive responses have been made from the use of Arabidopsis thaliana . In this special review, we will discuss results gleaned from reverse and forward genetic studies that revealed the involvement of both ABA‐dependent and ABA‐independent components. In particular, mutant analyses have highlighted the surprising prevalence of RNA metabolism in many key steps. We will also discuss our recent use of infrared thermography to visualize stomatal closure in response to dehydration as a means to identify novel regulatory genes. This has allowed us to recover mutations belonging to at least eight complementation groups. Analysis of six of these loci revealed that all of their corresponding mutations affect either abscisic acid (ABA) biosynthesis or perception. Hence, in contrast to molecular studies on gene networks which pointed to the clear existence of multiple ABA‐independent pathways in the control of dehydration tolerance, our results reinforce ABA‐based signalling pathways as the predominant factor in primary or rapid responses. Finally, we will provide some details learned from the molecular analysis of OPEN STOMATA1 ( OST1 ), a gene that encodes an ABA‐activated kinase issued from this targeted genetic approach.