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Understanding the function of the hypoxia-inducible transcription factor AtLBD41 and its homologs

Subject Area Plant Physiology
Term from 2018 to 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 417753486
 
Increasing number and duration of flooding events and drought periods, owing to climate change, lead to dramatic yield losses in crop plants. It is important to understand plant response mechanisms to flooding and the accompanying oxygen deficiency stress, as well as their regulation, in order to improve flooding tolerance of crop plants. In this project, we propose to characterize a transcriptional regulator, AtLBD41, which is among the strongly induced transcription factors under hypoxia in the model plant Arabidopsis thaliana. However, its function is currently unknown. Since it is also highly expressed under oxygen deficiency conditions in all other plant species analysed so far, it must have an important function in transcriptional regulation under this stress condition. The occurrence of an EAR domain in its sequence, together with a reported interaction with the co-repressor TOPLESS suggest that AtLBD41 is a repressor. Genes that are downregulated under oxygen deficiency are seldom the focus of studies, and hardly anything is known on the regulatory pathways. We have identified putative target genes of AtLBD41 and its homolog AtLBD40. Most likely, the third homolog AtLBD42 has a similar function, although it is hardly expressed in wildtype plants. Therefore we will create a triple lbd40/41/42 knockout for further studies. Putative target genes will be verified and new ones will be identified, e.g. by use of transcriptomics and protoplast transactivation assays. Second, we will ascertain the function of target genes under hypoxia and re-aeration as well as submergence, through physiological and biochemical experiments with the triple mutant and lines overexpressing an activating version of AtLBD41. The interaction of AtLBD41 with TOPLESS suggests the involvement of chromatin modifications in transcriptional repression through AtLBD41. We will therefore study these modifications on promoters of target genes under hypoxia in wildtype and mutant plants. Furthermore, interaction of AtLBD41 with SUMO-related enzymes has been shown, and we could demonstrate SUMOylation of AtLBD41. Consequently, we will study the effect of SUMOylation of AtLBD41 or its absence on protein stability, localization and function.
DFG Programme Research Grants
 
 

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