In complex, constantly changing environments, plants have developed astonishing survival strategies. These elaborated strategies rely on rapid and precise gene regulation mediated by transcription factors （TFs）. TFs...In complex, constantly changing environments, plants have developed astonishing survival strategies. These elaborated strategies rely on rapid and precise gene regulation mediated by transcription factors （TFs）. TFs represent a large fraction of plant genomes and among them, MYBs and basic helix-loop-helix （bHLHs） have unique inherent properties specific to plants. Proteins of these two TF families can act as homo- or heterodimers, associate with proteins from other protein families, or form MYB/bHLH complexes to regulate distinct cellular processes. The ability of MYBs and bHLHs to interact with multiple protein part- ners has evolved to keep up with the increased metabolic complexity of multi-cellular organisms. Associ- ation and disassociation of dynamic TF complexes in response to developmental and environmental cues are controlled through a plethora of regulatory mechanisms specifically modulating TF activity. Regulation of TFs at the protein level is critical for efficient and precise control of their activity, and thus provides the mechanistic basis for a rapid on-and-off switch of TF activity. In this review, examples of post-translational modifications, protein-protein interactions, and subcellular mobilization of TFs are discussed with regard to the relevance of these regulatory mechanisms for the specific activation of MYBs and bHLHs in response to a given environmental stimulus.展开更多
Survival in changing and challenging environments requires an organism to efficiently obtain and use its resources. Due to their sessile nature, it is particularly critical for plants to dynamically optimize their met...Survival in changing and challenging environments requires an organism to efficiently obtain and use its resources. Due to their sessile nature, it is particularly critical for plants to dynamically optimize their meta- bolism. In plant primary metabolism, metabolic fine-tuning involves feed-back mechanisms whereby the output of a pathway controls its input to generate a precise and robust response to environmental changes. By contrast, few studies have addressed the potential for feed-back regulation of secondary metabolism. In Arabidopsis, accumulation of the defense compounds glucosinolates has previously been linked to genetic variation in the glucosinolate biosynthetic gene AOP2. AOP2 expression can increase the transcript levels of two known regulators （MYB28 and MYB29） of the pathway, suggesting thatAOP2 plays a role in positive feed-back regulation controlling glucosinolate biosynthesis. We generated mutants affecting AOP2, MYB28/29, or both. Transcriptome analysis of these mutants identified a so far unrecognized link between AOP2 and jasmonic acid （JA） signaling independent of MYB28 and MYB29. Thus, AOP2 is part of a regulatory feed-back loop linking glucosinolate biosynthesis and JA signaling and thereby allows the glucosinolate pathway to influence JA sensitivity. The discovery of this regulatory feed-back loop provides insight into how plants optimize the use of resources for defensive metabolites.展开更多
文摘In complex, constantly changing environments, plants have developed astonishing survival strategies. These elaborated strategies rely on rapid and precise gene regulation mediated by transcription factors （TFs）. TFs represent a large fraction of plant genomes and among them, MYBs and basic helix-loop-helix （bHLHs） have unique inherent properties specific to plants. Proteins of these two TF families can act as homo- or heterodimers, associate with proteins from other protein families, or form MYB/bHLH complexes to regulate distinct cellular processes. The ability of MYBs and bHLHs to interact with multiple protein part- ners has evolved to keep up with the increased metabolic complexity of multi-cellular organisms. Associ- ation and disassociation of dynamic TF complexes in response to developmental and environmental cues are controlled through a plethora of regulatory mechanisms specifically modulating TF activity. Regulation of TFs at the protein level is critical for efficient and precise control of their activity, and thus provides the mechanistic basis for a rapid on-and-off switch of TF activity. In this review, examples of post-translational modifications, protein-protein interactions, and subcellular mobilization of TFs are discussed with regard to the relevance of these regulatory mechanisms for the specific activation of MYBs and bHLHs in response to a given environmental stimulus.
文摘Survival in changing and challenging environments requires an organism to efficiently obtain and use its resources. Due to their sessile nature, it is particularly critical for plants to dynamically optimize their meta- bolism. In plant primary metabolism, metabolic fine-tuning involves feed-back mechanisms whereby the output of a pathway controls its input to generate a precise and robust response to environmental changes. By contrast, few studies have addressed the potential for feed-back regulation of secondary metabolism. In Arabidopsis, accumulation of the defense compounds glucosinolates has previously been linked to genetic variation in the glucosinolate biosynthetic gene AOP2. AOP2 expression can increase the transcript levels of two known regulators （MYB28 and MYB29） of the pathway, suggesting thatAOP2 plays a role in positive feed-back regulation controlling glucosinolate biosynthesis. We generated mutants affecting AOP2, MYB28/29, or both. Transcriptome analysis of these mutants identified a so far unrecognized link between AOP2 and jasmonic acid （JA） signaling independent of MYB28 and MYB29. Thus, AOP2 is part of a regulatory feed-back loop linking glucosinolate biosynthesis and JA signaling and thereby allows the glucosinolate pathway to influence JA sensitivity. The discovery of this regulatory feed-back loop provides insight into how plants optimize the use of resources for defensive metabolites.
