Abstract
AbstractFlooding impairs plant growth through oxygen deprivation, which activates plant survival and acclimation responses. Low-oxygen responses are generally associated with activation of group VII ETHYLENE-RESPONSE FACTOR (ERFVII) transcription factors. However, mechanism and molecular components by which ERFVII factors initiate gene expression are not fully elucidated. Here, we show that the Mediator complex subunitAtMED25 is recruited by RELATED TO APETALA 2.2 (RAP2.2) and RAP2.12 to coordinate gene expression during hypoxia inArabidopsis thaliana.. Themed25mutants display reduced low-oxygen stress tolerance.AtMED25 associates with several ERFVII-controlled hypoxia core genes and its loss impairs transcription under hypoxia due to decreasing RNA polymerase II recruitment. Protein complex pulldown assays demonstrate that the Mediator complex built aroundAtMED25 is adjusted under low-oxygen conditions. Moreover, during hypoxia, no functional cooperation betweenAtMED25 and the two subunitsAtMED8 andAtMED16 occurs, contrasting previous observations made for other conditions. In addition,AtMED25 function under hypoxia is independent from ethylene signalling. Finally, a functional conservation at the molecular level was found for the MED25-ERFVII module betweenArabidopsis thalianaand the monocotOryza sativa, pointing to a potentially universal role of MED25 in enabling ERFVII-dependent transcript responses to hypoxia in plants.
Publisher
Cold Spring Harbor Laboratory
Cited by
1 articles.
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