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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.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE52298 | GEO | 2015/03/31

SECONDARY ACCESSION(S): PRJNA229087

REPOSITORIES: GEO

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Expression data from Arabidopsis myb3r mutants

Project description: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.

2015-03-31 | E-GEOD-52298 | biostudies-arrayexpress

Genome-wide identification of MYB3R3-bound genes

Project description:Arabidopsis genome has 5 genes that encode for R1R2R3-type Myb transcription factors. We showed previously that two R1R2R3-Myb transcriptional factors, MYB3R1 and MYB3R4, bind to cis-acting motifs called MSA, which are commonly present in many G2/M-specific genes and act as transcriptional activator. Here, we performed genome-wide approach to identify target genes of MYB3R3, which, together with MYB3R1 and MYB3R5, have potential functions in transcriptional repression of G2/M-specific genes. Our ChIP-seq analysis revealed that MYB3R3 preferentially binds to the G2/M-specific genes in vivo. In addition, our data also showed that MYB3R3 associates with the predicted target genes of E2F, well known transcription factors acting during G1/S. These results suggested that MYB3R3 may not only directly bind G2/M-specific genes though recognition of the MSA elements, but also indirectly associates with DNA replication genes through physical interaction with E2F.

2015-06-01 | GSE60554 | GEO

Overexpression of NtmybA2 in tobacco BY-2 cells

Project description:Promoters of many G2/M phase-specific genes in plants contain mitosis-specific activator (MSA) elements, which act as G2/M phase-specific enhancers and bind with R1R2R3-Myb transcription factors. A least three R1R2R3-Myb proteins are expressed in tobacco (Nicotiana tabacum). To examine the genome-wide effects of NtmybA2 overexpression, we constructed transgenic tobacco BY-2 cell lines overexpressing full-length NtmybA2 protein. In addition, we generated transgenic BY-2 cell lines that overexpress truncated hyperactive form of NtmybA2 (NtmybA2âC) lacking its C-terminal region which negatively regulates its own activity for transcriptional activation. We used a custom-made 16K cDNA microarray for comparative transcriptome analysis of these transgenic tobacco BY-2 cell lines. As control sample, BY-2 cells transformed with empty vector pPZP-35S were used. The transgenic cell lines were analyzed during stationary phase (i.e. day 7-8 after subculture into fresh media). Keywords: Genetic modification 1. pPZP-35S vector control, 2. NtmybA2 overexpressor, 3. C-truncated NtmybA2 (NtmyA2âC) overexpressor

2010-05-22 | E-GEOD-14251 | biostudies-arrayexpress

Overexpression of NtmybA2 in tobacco BY-2 cells

Project description:Promoters of many G2/M phase-specific genes in plants contain mitosis-specific activator (MSA) elements, which act as G2/M phase-specific enhancers and bind with R1R2R3-Myb transcription factors. A least three R1R2R3-Myb proteins are expressed in tobacco (Nicotiana tabacum). To examine the genome-wide effects of NtmybA2 overexpression, we constructed transgenic tobacco BY-2 cell lines overexpressing full-length NtmybA2 protein. In addition, we generated transgenic BY-2 cell lines that overexpress truncated hyperactive form of NtmybA2 (NtmybA2∆C) lacking its C-terminal region which negatively regulates its own activity for transcriptional activation. We used a custom-made 16K cDNA microarray for comparative transcriptome analysis of these transgenic tobacco BY-2 cell lines. As control sample, BY-2 cells transformed with empty vector pPZP-35S were used. The transgenic cell lines were analyzed during stationary phase (i.e. day 7-8 after subculture into fresh media). Keywords: Genetic modification

2009-02-28 | GSE14251 | GEO

Transcriptomic analysis of the myb3r1 myb3r4 double mutant in Arabidopsis thaliana

Project description:R1R2R3-Myb proteins represent an evolutionarily conserved class of Myb family proteins important for cell cycle regulation and differentiation in eukaryotic cells. In plants, this class of Myb proteins are believed to play important roles in cell cycle regulation through transcriptional regulation of G2/M phase-specific genes by binding to common cis-elements, called MSA elements. In Arabidopsis thaliana, MYB3R1 and MYB3R4 act as transcriptional activators and positively regulate cytokinesis by activating transcription of KNOLLE, which encodes a cytokinesis-specific syntaxin. Here, we show that the double mutation myb3r1 myb3r4 causes pleiotropic developmental defects, some of which are due to deficiency of KNOLLE whereas other are not, suggesting multiple target genes are involved. Consistently, microarray analysis of the double mutant revealed altered expression of many genes, among which G2/M-specific genes showed significant overrepresentation of the MSA motif and a strong tendency to be down-regulated by the double mutation. Our results demonstrate, on a genome-wide level, the importance of the MYB3R-MSA pathway for regulating G2/M-specific transcription. In addition, MYB3R1 and MYB3R4 may have diverse roles during plant development by regulating G2/M-specific genes with various functions, as well as genes possibly unrelated to the cell cycle. Comparison between the myb3r1 myb3r4 double mutant and wild type in three paired replicates.

2011-09-06 | E-GEOD-29433 | biostudies-arrayexpress

Transcriptomic analysis of the myb3r1 myb3r4 double mutant in Arabidopsis thaliana

2011-09-07 | GSE29433 | GEO

The MybMuvB complex is required for YAP dependent transcription of mitotic genes

Project description:YAP/TAZ, downstream effectors of the Hippo pathway, are important regulators of proliferation. Here we show that the ability of YAP to activate mitotic gene expression is dependent on the Myb-MuvB (MMB) complex, a master regulator of genes expressed in the G2/M phase of the cell cycle. By carrying out genome-wide expression and binding analyses, we found that YAP promotes binding of the MMB subunit B-MYB to the promoters of mitotic target genes. YAP binds to B-MYB and stimulates B-MYB chromatin-association through distal enhancer elements that interact with MMB-regulated promoters through chromatin looping. The cooperation between YAP and B-MYB is critical for YAP-mediated entry into mitosis. Furthermore, the expression of genes co-activated by YAP and B-MYB is associated with poor survival of cancer patients. Together, our findings provide a molecular mechanism by which YAP and MMB regulate mitotic gene expression and suggest a link between two cancer-relevant signaling pathways.

2019-06-18 | GSE115787 | GEO

A-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation

Project description:A-MYB (MYBL1) is a transcription factor with a role in meiosis in spermatocytes. The related B-MYB protein is a key proto-oncogene and a master regulator activating late cell cycle genes. To activate genes, B-MYB forms a complex with MuvB and is recruited indirectly to cell cycle genes homology region (CHR) promoter sites of target genes. Activation through the B-MYB-MuvB (MMB) complex is essential for successful mitosis. Here, we discover that A-MYB has a function in transcriptional regulation of the mitotic cell cycle and can substitute for B-MYB. Knockdown experiments in cells not related to spermatogenesis show that B-MYB loss alone only delays cell cycle progression. Only dual knockdown of B-MYB and A-MYB causes cell cycle arrest. A-MYB can substitute for B-MYB in binding to MuvB. The resulting A-MYB-MuvB complex activates genes through CHR sites. We find that A-MYB activates the same target genes as B-MYB. Many of the corresponding proteins are central regulators of the cell division cycle. In summary, we demonstrate that A-MYB is an activator of the mitotic cell cycle by activating late cell cycle genes.

2024-02-29 | GSE240799 | GEO

Gene expression profiling by array of human non-transformed RPE-FUCCI (Fluorescent Ubiquitination-based Cell Cycle Indicator) cells

Project description:Progression through the cell cycle is driven by cyclin dependent kinases that control gene expression, orchestration of the mitotic spindle and cell division. Here we used a Fluorescent Ubiquitination-based Cell Cycle Indicator (FUCCI) and performed transcriptomic analysis of human non-transformed cells. Cell sorting allowed efficient isolation of G1, S and G2 cells from asynchronously growing cell cultures. Altogether, we identified 701 differentially expressed genes in G1 and G2 cells.

2021-04-06 | E-MTAB-9626 | biostudies-arrayexpress

Structure and molecular assembly of a MuvB transcription factor complex with the nucleosome

Project description:The core cell cycle machinery genes are transcriptionally regulated by the MuvB family of protein complexes in a cell cycle specific manner. During cell cycle exit in quiescence or senescence, the DREAM complex, which is the repressive form of MuvB, directs transcriptional repression of cell cycle genes; conversely during cell proliferation, the complex of MuvB with the transcription factors (TFs) B-MYB and FOXM1 activate mitotic genes during the G2 phase of the cell cycle. The mechanisms of transcriptional regulation of these complexes are still poorly characterised. Here we combine biochemical analysis and in vitro reconstitution, with structural analysis by cryo-electron microscopy (cryo-EM) and cross-linking mass spectrometry (XL-MS), to functionally examine these complexes. Our data suggests that MuvB is a chromatin regulator whereby a core region binds the nucleosome and remodels it, thereby exposing nucleosomal DNA. This remodelling activity is supported by B-MYB which directly binds the remodelled DNA. Given the remodelling activity on the nucleosome, we propose that the MuvB complex with B-MYB (MMB) function as a pioneer transcription factor complex. Our data rationalises prior biochemical and cellular studies and provides a molecular framework of interactions on a protein complex, which is key for cell cycle regulation.

2022-08-17 | PXD031421 | Pride

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