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APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation

ABSTRACT: The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE48793 | GEO | 2013/11/04

SECONDARY ACCESSION(S): PRJNA211796

REPOSITORIES: GEO

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APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation

Project description:The quiescent center (QC) plays an essential role during root development by creating a microenvironment that preserves the stem cell fate of its surrounding cells. Strikingly, in order to retain root structure, QC cells only occasionally self-renew, displaying a proliferation rate far below that of all other cells within the root meristem. Previously, the APC/CCCS52A2 ubiquitine ligase and brassinosteroid signaling pathways have been found to antagonistically control Arabidopsis thaliana QC cell proliferation. Here, we demonstrate that both pathways converge on the ERF115 transcription factor that acts as a rate-limiting factor of QC cell division through transcriptional control of the autocrine phytosulfokine PSK5 peptide hormone. ERF115 marks QC cell division but is restrained through proteolysis by the APC/CCCS52A2 ubiquitine ligase, whereas QC proliferation is driven by brassinosteroid-dependent ERF115 expression. Combined, these two antagonistic mechanisms delimit the ERF115-PSK5 activity and QC renewal. Our results reveal a unique cell cycle regulatory mechanism that accounts for the low proliferation rate of QC cells within a surrounding population of highly mitotic active cells. ChIP-seq analysis of genes bound by the ERF115 transcription factor, using mock ChIP with wild type cells as negative control. Analyzed by Illumina HiSeq

2013-11-04 | E-GEOD-48793 | biostudies-arrayexpress

Transcript profiling of ERF115 transgenic Arabidopsis thaliana

2013-11-04 | GSE48836 | GEO

Transcript profiling of ERF115 transgenic Arabidopsis thaliana

Project description:This experiment was set up in order to identify the (direct) transcriptional targets of the Ethylene Response Factor 115 (ERF115) transcription factor. Because ERF115 expression occurs in quiescent center (QC) cells and strong effects on the QC cells were observed in ERF115 overexpression plants, root tips were harvested for transcript profiling in order to focus on root meristem and QC specific transcriptional targets. Wild-type (Col-0 ecotype), erf115 mutant (SALK_021981) and ERF115 overexpressing (p35S:ERF115 ORF) root tips (three replicates each) were harvested and subjected to transcript profiling, using the Col-0 samples as control reference.

2013-11-04 | E-GEOD-48836 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:APC/CCCS52A2 repressed phytosulfokine signaling restricts root QC cell proliferation through ERF115 degradation

| PRJNA211796 | ENA

A Mobile miR160-Triggered Transcriptional Axis Controls Root Stem Cell Niche Maintenance and Regeneration in Arabidopsis

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.

2024-09-27 | GSE255979 | GEO

A single-cell morpho-transcriptomic map of brassinosteroid action in the Arabidopsis root

Project description:The effects of brassinosteroid signaling on shoot and root development have been characterized in great detail but did not identify a simple consistent positive or negative impact on a basic cellular parameter. Here we combined digital 3D single-cell shape analysis and single-cell mRNA sequencing to characterize root meristems and mature root segments of brassinosteroid-blind mutants and wildtype. These data demonstrate that brassinosteroid signaling neither affects cell volume nor cell proliferation capacity. Instead, brassinosteroid signaling is essential for the precise orientation of cell division planes and the extent and timing of anisotropic cell expansion. Moreover, we found that the cell-aligning effects of brassinosteroid signaling can propagate to normalize the anatomy of both adjacent and distant brassinosteroid-blind cells through non-cell-autonomous functions, which are sufficient to restore growth vigor. Finally, single-cell transcriptome data discern directly brassinosteroid-responsive genes from genes that can react non-cell-autonomously and highlight arabinogalactans as sentinels of brassinosteroid-dependent anisotropic cell expansion.

2021-08-23 | GSE181178 | GEO

Precise transcriptional control of cellular quiescence by BRAVO/WOX5 complex in Arabidopsis roots

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.

2021-05-06 | GSE173945 | GEO

The ubiquitin E3 ligase APC/CCdc20 mediates mitotic degradation of OGT

Project description:O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT) is the sole enzyme that catalyzes all O-GlcNAcylation reactions intracellularly. Previous investigations have found that OGT levels oscillate during the cell division process. Specifically, OGT abundance is downregulated during mitosis, but the underlying mechanism is lacking. Here we demonstrate that OGT is ubiquitinated by the ubiquitin E3 ligase, anaphase promoting complex/cyclosome (APC/C)-cell division cycle 20 (Cdc20). We show that APC/CCdc20 interacts with OGT through a conserved destruction box (D-box): Arg-351/Leu-354, the abrogation of which stabilizes OGT. As APC/CCdc20-substrate binding is often preceded by a priming ubiquitination event, we also used mass spectrometry and mapped OGT Lys-352 to be a ubiquitination site, which is a prerequisite for OGT association with APC/C subunits. Interestingly in The Cancer Genome Atlas, R351C is a uterine carcinoma mutant, suggesting that mutations of the D-box are linked with tumorigenesis. Paradoxically, we found that both R351C and the D-box mutants (R351A/L354A) inhibit uterine carcinoma in mouse xenograft models, probably due to impaired cell division and proliferation. In sum, we propose a model where OGT Lys-352 ubiquitination primes its binding with APC/C, and then APC/CCdc20 partners with OGT through the D-box for its mitotic destruction. Our work not only highlights the key mechanism that regulates OGT during the cell cycle, but also reveals the mutual coordination between glycosylation and the cell division machinery.

2024-08-10 | PXD050552 | Pride

Microtubule-associated CLASP balances brassinosteroid signaling through negative feedback to sustain plant cell proliferation

Project description:The capacity for sustained cell division is a critical determinant of plant meristem development, and ultimately, organ size. This capacity is diminished in mutants lacking the microtubule-associated protein CLASP, and when brassinosteroid signaling is increased. Here, we discovered that CLASP is both targeted by and promotes activity of the brassinosteroid pathway in Arabidopsis root apical meristems. We show that enhanced brassinosteroid signalling reduces CLASP transcript and protein levels, and dramatically shifts microtubule organization to promote exit from the cell division cycle. Notably, CLASP sustains brassinosteroid signalling by fostering retrieval of endocytosed BRI1 receptors to the plasma membrane through the tethering of SNX1 vesicles to microtubules. clasp-1 null mutants have fewer BRI1 receptors, and impaired BR-mediated transcriptional activity and responses. Global transcript profiling confirmed the collapse of cell cycle activity in clasp-1 and revealed hormone crosstalk. Together, these findings reveal an unprecedented form of negative feedback that supports meristem homeostasis.

2017-05-01 | GSE85262 | GEO

Anaphase-promoting complex-dependent control of cell identity

Project description:Tissue development and homeostasis rely on the proliferation of progenitor cells, whose identities are established by tightly controlled gene expression networks. However, mRNA synthesis is inhibited during mitosis, and the transcriptional programs that define a cell type must be restarted upon entry into each new cell cycle; how this is accomplished is poorly understood. Here, we identified a ubiquitin-dependent mechanism that integrates gene expression with cell division to preserve cell identity. We found that WDR5 and TBP, which bind active promoters during interphase, recruit the E3 ligase anaphase-promoting complex (APC/C) to specific transcription start sites during mitosis. This allows the APC/C to locally decorate histones with K11/K48-linked ubiquitin chains, which destabilizes nucleosomes and ensures continued gene expression in the next cell cycle. Mitotic exit and transcription re-initiation are therefore controlled by the same essential regulator, the APC/C, which provides a robust mechanism to maintain cell identity through cell division.

2020-02-03 | GSE122298 | GEO

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