Precise transcriptional control of cellular quiescence by BRAVO/WOX5 complex in Arabidopsis roots
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ABSTRACT:
PROVIDER: PRJNA727585 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14434341.fastq.gz | Fastqsanger.gz | |||
| SRR14434342.fastq.gz | Fastqsanger.gz | |||
| SRR14434343.fastq.gz | Fastqsanger.gz | |||
| SRR14434344.fastq.gz | Fastqsanger.gz | |||
| SRR14434345.fastq.gz | Fastqsanger.gz |
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Project description:Understanding stem cell regulatory circuits is the next challenge in plant biology, as these cells are essential for tissue growth and organ regeneration in response to stress. In the Arabidopsis primary root apex, stem-cell specific transcription factors BRAVO and WOX5 co-localize in the Quiescent Center (QC) cells, where they commonly repress cell division so that these cells can act as a reservoir to replenish surrounding stem cells, yet their molecular connection remains unknown. Genetic and biochemical analysis indicates that BRAVO and WOX5 form a transcription factor complex that modulates gene expression in the QC cells to preserve overall root growth and architecture. Furthermore, by using mathematical modeling we establish that BRAVO uses the WOX5/BRAVO complex to promote WOX5 activity in the stem cells. Our results unveil the importance of transcriptional regulatory circuits in plant stem cell development.
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Project description:Understanding stem cell regulatory circuits is the next challenge in plant biology, as these cells are essential for tissue growth and organ regeneration in response to stress. In the Arabidopsis primary root apex, stem cell-specific transcription factors BRAVO and WOX5 co-localize in the quiescent centre (QC) cells, where they commonly repress cell division so that these cells can act as a reservoir to replenish surrounding stem cells, yet their molecular connection remains unknown. Genetic and biochemical analysis indicates that BRAVO and WOX5 form a transcription factor complex that modulates gene expression in the QC cells to preserve overall root growth and architecture. Furthermore, by using mathematical modelling we establish that BRAVO uses the WOX5/BRAVO complex to promote WOX5 activity in the stem cells. Our results unveil the importance of transcriptional regulatory circuits in plant stem cell development.
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Project description:4plex_brachy_2016_01 - vasc1-bravo - Are hormone signaling genes misregulated in VASC1. - During a screening of the Brachypodium mutant collection at Versailles, a line was identified with a marked vascular phenotype. The causal locus segregates Mendelian way (a recessive locus). A candidate gene was identified by ILLUMINA sequencing at the Joint Genome Institute (JGI) and by the ShoreMAP technique. The objective is to identify which genes whose expression is deregulated in this mutant explain the observed phenotype.
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Project description:In multicellular organisms, communication between cells is vital for their fate determination. In plants, the quiescent center (QC) signals to adjacent stem cells to maintain them undifferentiated. However, how surrounding stem cells instruct the QC remains poorly understood. Here we show that in the Arabidopsis root, microRNA160 (miR160) moves from vascular stem cells to the QC, where it degrades the mRNAs of two auxin response factors, ARF10 and ARF17. This degradation relieves BRAVO from direct transcriptional repression, maintaining QC quiescence. We further identify that blocking miR160 movement due to DNA damage-induced vascular stem cell death and restricted symplastic transport reduces BRAVO and WOX5 expression, leading to QC division to replenish damaged stem cells during root regeneration. Together, our results demonstrate that a transcriptional axis initiated by mobile miR160 regulates the QC and stem cell behavior, advancing our understanding of the communication between stem cells and their surrounding cellular environment.
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Project description:Cellular quiescence is coupled with cellular development, tissue homeostasis, and cancer progression. Both quiescence and cell cycle re-entry are controlled by active and precise regulation of gene expression. However, the roles of long noncoding RNAs (lncRNAs) during these processes remain to be elucidated. By performing a genome-wide transcriptome analyses, we identify thousands of differentially expressed lncRNAs, including ~30 of the less-characterized class of microRNA-host-gene lncRNAs (lnc-MIRHGs), during cellular quiescence and during serum-stimulation in human diploid cells. We observe that the mature MIR222HG display serum-stimulated induction due to enhanced pre-RNA splicing. Serum-stimulated binding of the pre-mRNA splicing factor SRSF1 to a micro-exon, which partially overlaps with the primary miR-222 precursor, facilitates enhanced MIR222HG splicing. In serum-stimulated cells, SRSF1 negatively regulates the Drosha/DGCR8-catalyzed cleavage of pri-miR-222, thereby increasing the cellular pool of the mature MIR222HG. Further, loss-of-function studies indicate that the mature MIR222HG facilitates the serum-stimulated cell cycle re-entry in a microRNA-independent manner. Mechanistically, MIR222HG, along with ILF3/2 complex, forms RNA:RNA duplex with DNM3OS lncRNA, thereby promoting DNM3OS stability. The current study identifies a mechanism in which the interplay between splicing versus microprocessor complex dictates the serum-induced expression of lnc-MIRHG MIR222HG for efficient cell cycle re-entry.
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Project description:Transition from proliferation to quiescence brings about extensive changes in cellular behavior and structure. However, genes critical for establishing and/or for maintaining quiescence are largely unknown. The fission yeast S. pombe is found as an excellent model for studying this problem, because it becomes quiescent under nitrogen starvation. Here we characterize 610 temperature-sensitive (ts) mutants, and identify 33 genes required for entry into and the maintenance of quiescence. These genes cover a broad range of cellular functions in the cytoplasm, membrane and the nucleus, encoding proteins for stress-responsive and cell cycle kinase signaling pathway, actin-bound and osmo-controlling endosome formation, RNA transcription, splicing and ribosome biogenesis, chromatin silencing, biosynthesis of lipid and ATP, cell wall and membrane morphogenesis, protein trafficking and vesicle fusion. We specifically highlight Fcp1, CTD phosphatase of RNA polymerase II, which differentially affects transcription of genes involved in quiescence and proliferation. We propose that the transcriptional role of Fcp1 is central to differentiate quiescence from proliferation. Keywords: cell cycle control, protein trafficking, cortex actin, RNA polymerase II, protein phosphatase
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