4.8 Article

AUXIN RESPONSE FACTOR 18-HISTONE DEACETYLASE 6 module regulates floral organ identity in rose (Rosa hybrida)

Journal

PLANT PHYSIOLOGY
Volume 186, Issue 2, Pages 1074-1087

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/plphys/kiab130

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Funding

  1. National Key Research and Development Program (Ministry of Science and Technology of the People's Republic of China) [2018YFD1000400]
  2. National Natural Science Foundation of China [31730079, 31872148]
  3. Construction of Beijing Science and Technology Innovation and Service Capacity in Top Subjects (Beijing Municipal Education Commission) [CEFF-PXM2019_014207_000032]
  4. 111 Project (Ministry of Education of the People's Republic of China) [B17043]

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Auxin levels influence floral organ identity in rose by regulating the expression of genes such as RhPILS1 and RhARF18, which control the homeotic transformation between petals and stamens. RhARF18 interacts with RhHDA6 to repress the transcription of RhAG, ultimately impacting petal number in floral development.
The phytohormone auxin plays a pivotal role in floral meristem initiation and gynoecium development, but whether and how auxin controls floral organ identity remain largely unknown. Here, we found that auxin levels influence organ specification, and changes in auxin levels influence homeotic transformation between petals and stamens in rose (Rosa hybrida). The PIN-FORMED-LIKES (PILS) gene RhPILS1 governs auxin levels in floral buds during floral organogenesis. RhAUXIN RESPONSE FACTOR 18 (RhARF18), whose expression decreases with increasing auxin content, encodes a transcriptional repressor of the C-class gene RhAGAMOUS (RhAG), and controls stamen-petal organ specification in an auxin-dependent manner. Moreover, RhARF18 physically interacts with the histone deacetylase (HDA) RhHDA6. Silencing of RhHDA6 increases H3K9/K14 acetylation levels at the site adjacent to the RhARF18-binding site in the RhAG promoter and reduces petal number, indicating that RhARF18 might recruit RhHDA6 to the RhAG promoter to reinforce the repression of RhAG transcription. We propose a model for how auxin homeostasis controls floral organ identity via regulating transcription of RhAG

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