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Roles of mitochondrial energy dissipation systems in plant development and acclimation to stress
Xiaojun Pu1, Xin Lv1, Tinghong Tan1
1Ministry of Education Key Laboratory for Bio-Resource & Eco-Environment and Plant Physiology Laboratory, College of Life Science, State Key Laboratory of Hydraulics and Mountain River Engineering, Sichuan University, Chengdu 610064, China.
Background:
Plants are sessile organisms that have the ability to integrate external cues into metabolic and developmental signals. The cues initiate specific signal cascades that can enhance the tolerance of plants to stress, and these mechanisms are crucial to the survival and fitness of plants. The adaption of plants to stresses is a complex process that involves decoding stress inputs as energy-deficiency signals. The process functions through vast metabolic and/or transcriptional reprogramming to re-establish the cellular energy balance. Members of the mitochondrial energy dissipation pathway (MEDP), alternative oxidases (AOXs) and uncoupling proteins (UCPs), act as energy mediators and might play crucial roles in the adaption of plants to stresses. However, their roles in plant growth and development have been relatively less explored.
Scope:
This review summarizes current knowledge about the role of members of the MEDP in plant development as well as recent advances in identifying molecular components that regulate the expression of AOXs and UCPs. Highlighted in particular is a comparative analysis of the expression, regulation and stress responses between AOXs and UCPs when plants are exposed to stresses, and a possible signal cross-talk that orchestrates the MEDP, reactive oxygen species (ROS), calcium signalling and hormone signalling.
Conclusions:
The MEDP might act as a cellular energy/metabolic mediator that integrates ROS signalling, energy signalling and hormone signalling with plant development and stress accumulation. However, the regulation of MEDP members is complex and occurs at transcriptional, translational, post-translational and metabolic levels. How this regulation is linked to actual fluxes through the AOX/UCP in vivo remains elusive.
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