Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from Arabidopsis myb3r mutants


ABSTRACT: Temporal and spatial regulation of cell division is central for generating multicellular organs with predictable sizes and shapes. However, it remains largely unclear how genes with mitotic functions are transcriptionally regulated during organogenesis in plants. Here, we showed that a group of R1R2R3-Myb transcription factors are responsible for developmentally controlled downregulation of variety of mitotic genes in Arabidopsis. Loss of their functions resulted in elevated expression of mitotic genes in quiescent cells including those underwent terminal differentiation. Concomitantly, their mutations enhanced cell division activities in various aspects of plant development, generating organs with increased sizes and irregular architectures. In addition, we showed that this type of R1R2R3-Myb proteins are required for oscillated expression of G2/M-specfiic genes, most likely by inhibiting transcription outside of G2/M in the cell cycle. Our finding uncovered a novel plant-specific mechanism in which scheduled expression of G2/M-specific genes may require their global repression both in the cell cycle and during development. Seedlings (9d-old) or leaves (5d or 15d-old) of the wild type or myb3r mutants were sampled for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Misato Ohtani 

PROVIDER: E-GEOD-52298 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications


In multicellular organisms, temporal and spatial regulation of cell proliferation is central for generating organs with defined sizes and morphologies. For establishing and maintaining the post-mitotic quiescent state during cell differentiation, it is important to repress genes with mitotic functions. We found that three of the Arabidopsis MYB3R transcription factors synergistically maintain G2/M-specific genes repressed in post-mitotic cells and restrict the time window of mitotic gene express  ...[more]

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