BZR1 promotes pluripotency acquisition and callus development through direct regulation of ARF7 and ARF19

Author:

Ebstrup E,Ammitsøe T,Blanco-Touriñán N,Hansen J,Hardtke CSORCID,Rodriguez EORCID,Petersen MORCID

Abstract

AbstractPlants have the remarkable ability to regenerate whole organisms through formation of pluripotent cell masses from somatic cells. Cellular programs leading to fate change of somatic to pluripotent cells resembles lateral root (LR) formation and both are chiefly regulated by auxin. Brassinosteroid signalling also plays an important role during LR formation but little is known about the direct link between auxin and brassinosteroid components, such as BZR1 and BES1, in relation to pluripotency acquisition. Here we show that gain-of-function mutantsbzr1-Dandbes1-Dexhibit altered callus formation, yet disruption of these transcription factors does not produce major changes to callus formation orde novo organogenesis. Moreover, our data reveals that BZR1 displays enhanced expression in callus tissue and directly binds to the promoters of ARF7 and ARF19, two master pluripotency regulators, leading to their enhanced transcription. Remarkably, we see abrogation of callus formation inbzr1-Dupon disruption of ARF7 and ARF19, emphasizing that BZR1 callus phenotype is dependent on these two auxin signalling components. In conclusion, we depict a link between ARF7, ARF19 and BZR1 in the promotion of pluripotency acquisition, portraying BZR1 as a major supporting factor in callus formation.IMPORTANTManuscripts submitted to Review Commons are peer reviewed in a journal-agnostic way.Upon transfer of the peer reviewed preprint to a journal, the referee reports will be available in full to the handling editor.The identity of the referees will NOT be communicated to the authors unless the reviewers choose to sign their report.The identity of the referee will be confidentially disclosed to any affiliate journals to which the manuscript is transferred.GUIDELINESFor reviewers:https://www.reviewcommons.org/reviewersFor authors:https://www.reviewcommons.org/authorsCONTACTThe Review Commons office can be contacted directly at:office@reviewcommons.org

Publisher

Cold Spring Harbor Laboratory

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