Abstract
Author SummaryRespiratory metabolism in land plants requires oxygen availability to be able to generate ATP, which is essential for biosynthetic processes. Cellular hypoxia can be triggered as a consequence of environmental events (mainly floods), anatomical constraints (low tissue permeability to gases), or elevated cellular respiration, and it is unfavorable to growth due to the resultant decline in ATP. The adaptation of plants to fluctuating oxygen levels inside tissues requires the dynamic regulation of mechanisms that ensure cell viability and ultimately organism survival, but only a few molecular components of this homeostatic network are known. Direct hypoxia-sensing entails the posttranslational stabilization of a subgroup of plant ethylene-responsive factor (ERF) transcription factors, which coordinate the expression of hypoxia-inducible genes. Turnover of these ERFs is determined by an oxygen-dependent pathway of proteasomal degradation. Here, we demonstrate that the hypoxia-inducible transcription factor gene HRA1 is transcriptionally activated upon ERF-VII RAP2.12 stabilization and encodes a trihelix DNA binding protein that functionally interacts with RAP2.12 to curtail its activity. In addition to its negative regulation of RAP2.12, HRA1 negatively regulates activation of its own promoter. This RAP2.12-HRA1 control unit allows plants to modulate the extent of the response to hypoxia, including anaerobic enzyme production, to levels that improve endurance of the stress. Our results emphasize the importance of a strategy that can counterbalance energy-inefficient survival responses.
Highlights
In higher plants, respiratory metabolism requires molecular oxygen as the terminal electron acceptor to generate ATP
Direct hypoxia-sensing entails the posttranslational stabilization of a subgroup of plant ethylene-responsive factor (ERF) transcription factors, which coordinate the expression of hypoxia-inducible genes
We demonstrate that the hypoxia-inducible transcription factor gene HYPOXIA RESPONSE ATTENUATOR1 (HRA1) is transcriptionally activated upon ethylene-responsive factor group VII (ERF-VII) RAP2.12 stabilization and encodes a trihelix DNA binding protein that functionally interacts with RAP2.12 to curtail its activity
Summary
Respiratory metabolism requires molecular oxygen as the terminal electron acceptor to generate ATP. Limited oxygen availability (hypoxia) can occur in plant cells due to floods, frosts, and excessive respiration, requiring physiological acclimation to constraints in ATP availability for growth and development [1,2]. The switch from aerobic respiration to anaerobic ethanolic fermentation, as a means to maintain substrate-level ATP production from available carbohydrates, is essential for plant survival in conditions of oxygen deprivation [3,4]. On the other hand, uncontrolled or constitutive fermentation is detrimental to plant survival, due to rapid depletion of carbohydrate resources needed for basic cellular homeostasis [7]. Accurately balanced to meet plant requirements for survival under fluctuating oxygen conditions [9]
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