“…To identify specific ABA signaling components that are involved in after-ripening mediated seed dormancy decay in wheat, we compared the expression of 63 probesets annotated as genes related to ABA signaling between after-ripened and dormant seeds in both dry and imbibed states. Members of the ABA receptor PYR/PYL/RCAR family form a complex with ABA to induce ABA-response [57]. Consistently, seeds from plants overexpressing PYL8 / RCAR3 exhibit increased ABA sensitivity and enhanced dormancy [58], while those derived from loss of function mutants exhibit strong ABA insensitivity [17].…”
Treatments that promote dormancy release are often correlated with changes in seed hormone content and/or sensitivity. To understand the molecular mechanisms underlying the role of after-ripening (seed dry storage) in triggering hormone related changes and dormancy decay in wheat (Triticum aestivum), temporal expression patterns of genes related to abscisic acid (ABA), gibberellin (GA), jasmonate and indole acetic acid (IAA) metabolism and signaling, and levels of the respective hormones were examined in dormant and after-ripened seeds in both dry and imbibed states. After-ripening mediated developmental switch from dormancy to germination appears to be associated with declines in seed sensitivity to ABA and IAA, which are mediated by transcriptional repressions of PROTEIN PHOSPHATASE 2C, SNF1-RELATED PROTEIN KINASE2, ABA INSENSITIVE5 and LIPID PHOSPHATE PHOSPHTASE2, and AUXIN RESPONSE FACTOR and RELATED TO UBIQUITIN1 genes. Transcriptomic analysis of wheat seed responsiveness to ABA suggests that ABA inhibits the germination of wheat seeds partly by repressing the transcription of genes related to chromatin assembly and cell wall modification, and activating that of GA catabolic genes. After-ripening induced seed dormancy decay in wheat is also associated with the modulation of seed IAA and jasmonate contents. Transcriptional control of members of the ALLENE OXIDE SYNTHASE, 3-KETOACYL COENZYME A THIOLASE, LIPOXYGENASE and 12-OXOPHYTODIENOATE REDUCTASE gene families appears to regulate seed jasmonate levels. Changes in the expression of GA biosynthesis genes, GA 20-OXIDASE and GA 3-OXIDASE, in response to after-ripening implicate this hormone in enhancing dormancy release and germination. These findings have important implications in the dissection of molecular mechanisms underlying regulation of seed dormancy in cereals.
“…To identify specific ABA signaling components that are involved in after-ripening mediated seed dormancy decay in wheat, we compared the expression of 63 probesets annotated as genes related to ABA signaling between after-ripened and dormant seeds in both dry and imbibed states. Members of the ABA receptor PYR/PYL/RCAR family form a complex with ABA to induce ABA-response [57]. Consistently, seeds from plants overexpressing PYL8 / RCAR3 exhibit increased ABA sensitivity and enhanced dormancy [58], while those derived from loss of function mutants exhibit strong ABA insensitivity [17].…”
Treatments that promote dormancy release are often correlated with changes in seed hormone content and/or sensitivity. To understand the molecular mechanisms underlying the role of after-ripening (seed dry storage) in triggering hormone related changes and dormancy decay in wheat (Triticum aestivum), temporal expression patterns of genes related to abscisic acid (ABA), gibberellin (GA), jasmonate and indole acetic acid (IAA) metabolism and signaling, and levels of the respective hormones were examined in dormant and after-ripened seeds in both dry and imbibed states. After-ripening mediated developmental switch from dormancy to germination appears to be associated with declines in seed sensitivity to ABA and IAA, which are mediated by transcriptional repressions of PROTEIN PHOSPHATASE 2C, SNF1-RELATED PROTEIN KINASE2, ABA INSENSITIVE5 and LIPID PHOSPHATE PHOSPHTASE2, and AUXIN RESPONSE FACTOR and RELATED TO UBIQUITIN1 genes. Transcriptomic analysis of wheat seed responsiveness to ABA suggests that ABA inhibits the germination of wheat seeds partly by repressing the transcription of genes related to chromatin assembly and cell wall modification, and activating that of GA catabolic genes. After-ripening induced seed dormancy decay in wheat is also associated with the modulation of seed IAA and jasmonate contents. Transcriptional control of members of the ALLENE OXIDE SYNTHASE, 3-KETOACYL COENZYME A THIOLASE, LIPOXYGENASE and 12-OXOPHYTODIENOATE REDUCTASE gene families appears to regulate seed jasmonate levels. Changes in the expression of GA biosynthesis genes, GA 20-OXIDASE and GA 3-OXIDASE, in response to after-ripening implicate this hormone in enhancing dormancy release and germination. These findings have important implications in the dissection of molecular mechanisms underlying regulation of seed dormancy in cereals.
“…The knowledge accumulating on ABA signal transduction has been described in detail in many recently published reviews Hirayama and Shinozaki 2010;Hubbard et al 2010;Kline et al 2010;Klingler et al 2010;Melcher et al 2010;Muschietti and McCormick 2010;Raghavendra et al 2010;Umezawa et al 2010;Weiner et al 2010;Fujita et al 2011;Hauser et al 2011;Joshi-Saha et al 2011;Umezawa 2011). Most of these reviews have been based on the studies carried out on the model plant Arabidopsis.…”
The phytohormone abscisic acid (ABA) affects a wide range of stages of plant development as well as the plant's response to biotic and abiotic stresses. Manipulation of ABA signaling in commercial crops holds promising potential for improving crop yields. Several decades of research have been invested in attempts to identify the first components of the ABA signaling cascade. It was only in 2009, that two independent groups identified the PYR/PYL/RCAR protein family as the plant ABA receptor. This finding was followed by a surge of studies on ABA signal transduction, many of them using Arabidopsis as their model. The ABA signaling cascade was found to consist of a double-negative regulatory mechanism assembled from three protein families. These include the ABA receptors, the PP2C family of inhibitors, and the kinase family, SnRK2. It was found that ABA-bound PYR/RCARs inhibit PP2C activity, and that PP2Cs inactivate SnRK2s. Researchers today are examining how the elucidation of the ABA signaling cascade in Arabidopsis can be applied to improvements in commercial agriculture. In this article, we have attempted to review recent studies which address this issue. In it, we discuss various approaches useful in identifying the genetic and protein components involved. Finally, we suggest possible commercial applications of genetic manipulation of ABA signaling to improve crop yields.
“…The main consequence of this stomatal dysfunction is a reduced capacity of leaves to maintain an adequate water status, which often results in a lethal degree of water stress (Fanourakis et al , 2013 b ). Despite the recent advances in our understanding of signalling in guard cells (Nambara and Marion-Poll, 2005; Li et al , 2006; Kim et al , 2010; Kline et al , 2010; Raghavendra et al , 2010; Umezawa et al , 2010; Lee and Luan, 2012), the signal transduction elements which are disturbed or disrupted in guard cells of malfunctioning stomata are still not understood. As highlighted at âStomata 2012â (29th New Phytologist symposium, Manchester, UK), considering the impact of stomata on global issues, more information is required on environmental influences on guard cell responses (Roelfsema and Kollist, 2013).…”
The response of stomata to many environmental factors is well documented. Multiple signalling pathways for abscisic acid (ABA)-induced stomatal closure have been proposed over the last decades. However, it seems that exposure of a leaf for a long time (several days) to some environmental conditions generates a sort of memory in the guard cells that results in the loss of suitable responses of the stomata to closing stimuli, such as desiccation and ABA. In this review paper we discuss changes in the normal pattern of signal transduction that could account for disruption of guard cell signalling after long-term exposure to some environmental conditions, with special emphasis on long-term low vapour pressure deficit (VPD).
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