DOF2.1 controls vascular cell proliferation downstream of TMO5/LHW
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ABSTRACT:
PROVIDER: PRJNA480449 | ENA |
REPOSITORIES: ENA
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Project description:As plant cells are fixed within their tissue context, a precise control of cell division orientation is crucial to generate complex three-dimensional organs. The transcription factor complex formed by TARGET OF MONOPTEROS5 (TMO5) and LONESOME HIGHWAY (LHW) triggers a change in cell division orientation leading to radial expansion, at least in part by activating local cytokinin biosynthesis. However, it remains unclear how cytokinin controls these oriented cell divisions. Here, we analyzed the transcriptional responses upon simultaneous induction of both TMO5 and LHW in detail. Using inferred network analysis, we identify AT2G28510/DOF2.1 as a cytokinin-dependent downstream target gene of the TMO5/LHW heterodimer complex. We further show that DOF2.1 is specifically required and sufficient for vascular cell proliferation without inducing other cytokinin-dependent effects such as the inhibition of vascular differentiation. In summary, we have identified DOF2.1 as a TMO5/LHW target gene, specifically responsible for controlling vascular cell proliferation leading to radial expansion.
2019-01-24 | GSE116858 | GEO
Project description:TFEB controls vascular development by regulating the proliferation of endothelial cells
| PRJNA349032 | ENA
Project description:The final size and arrangement of the plant vasculature requires precise adjustment of cell proliferation. In particular, radial growth of vascular bundles is to a large extent controlled by a bHLH transcription factor heterodimer formed by TARGET OF MONOPTEROS5 (TMO5) and LONESOME HIGHWAY (LHW). Excess activity of this TMO5/LHW dimer causes excessive proliferation of vascular cell divisions and thus suggests the existence of a molecular mechanism that restricts its activity in space and time. Here we show that this overproliferation phenotype is similar to acaulis5 (acl5) mutants, suggesting a role for ACL5 in controlling TMO5/LHW activity. We further identify the clade of SAC51-LIKE (SACL) bHLH transcription factors whose translation is regulated by ACL5, as inhibitors of TMO5/LHW activity. We show that SACL proteins interact with LHW impairing activation of downstream targets and alleviating the overproliferation caused by TMO5/LHW misexpression. Given that transcription of SACL genes is induced by TMO5/LHW and its upstream trigger auxin, we propose that SACL proteins represent a feedback mechanism that limits activity of this pathway and controls periclinal cell divisions.
2015-09-01 | GSE70157 | GEO
Project description: Not available
| S-EPMC6370950 | biostudies-literature
Project description:The final size and arrangement of the plant vasculature requires precise adjustment of cell proliferation. In particular, radial growth of vascular bundles is to a large extent controlled by a bHLH transcription factor heterodimer formed by TARGET OF MONOPTEROS5 (TMO5) and LONESOME HIGHWAY (LHW). Excess activity of this TMO5/LHW dimer causes excessive proliferation of vascular cell divisions and thus suggests the existence of a molecular mechanism that restricts its activity in space and time. Here we show that this overproliferation phenotype is similar to acaulis5 (acl5) mutants, suggesting a role for ACL5 in controlling TMO5/LHW activity. We further identify the clade of SAC51-LIKE (SACL) bHLH transcription factors whose translation is regulated by ACL5, as inhibitors of TMO5/LHW activity. We show that SACL proteins interact with LHW impairing activation of downstream targets and alleviating the overproliferation caused by TMO5/LHW misexpression. Given that transcription of SACL genes is induced by TMO5/LHW and its upstream trigger auxin, we propose that SACL proteins represent a feedback mechanism that limits activity of this pathway and controls periclinal cell divisions. Three biological replicates were generated per sample. The goal of this experiment is to compare different genotypes that suppress the acl5 mutant as Columbia-0, acl5 + pHS::SACL3 and acl5 ajax2-31, against the acl5 mutant. Every pair of samples that were compared in the same array, were also growth in the same plate. The acl5 + pHS::SACL3 seedlings (and the acl5 ones against they are went compared) were treated to 37C degrees heat shock and then collected at the different times (30 and 210 min) after heat shock. In each comparison 1 or 2 or the replcates were reversed-labeled.
2015-09-01 | E-GEOD-70157 | biostudies-arrayexpress
Project description:Identification of regulators of vascular proliferation
| PRJNA490511 | ENA
Project description:Normal development requires tight regulation of cell proliferation and cell death. Here, we investigated these control mechanisms in the hyaloid vessels, a temporary vascular network in the mammalian eye that requires a Wnt/β-catenin response for scheduled regression. Transcriptome analysis of the postnatal day 5 mouse hyaloid showed expression of several Wnt pathway proteins. We investigated whether the hyaloid Wnt response was linked to the oncogene Myc, and the cyclin-dependent kinase inhibitor P21 (CDKN1A), both established regulators of cell cycle progression and cell death. Our analysis showed that the Wnt pathway coreceptors LRP5 and LRP6 have overlapping activities mediating the Wnt/β-catenin signaling in hyaloid vascular endothelial cells (VECs). We also showed that both Myc and Cdkn1a are downstream of the Wnt response and are required for hyaloid regression but for different reasons. Conditional deletion of Myc in VECs suppressed both proliferation and cell death. By contrast, conditional deletion of Cdkn1a resulted in VEC over-proliferation that countered the effects of cell death on regression. When combined with analysis of MYC, and P21 protein levels, this analysis suggests that a Wnt/β-catenin, MYC-P21 pathway regulates scheduled hyaloid vessel regression.
2018-06-15 | GSE113294 | GEO
Project description:Developmental vascular regression is regulated by a Wnt/b-catenin, MYC, P21 (CDKN1A) pathway that controls cell proliferation and cell death
| PRJNA450678 | ENA
Project description:6 timepoints: Day 0 (normal controls), progressively developing neointimal vascular proliferation and pulmonary hypertension in vehicle treated animals (Days 14, 21, 28 and 35) and triptolide-treated animals at Day 35. Replicates: 6 for Day 0 (normal) 2 for Daty 14 3 each for Days 21, 28, 35 and Triptolide -treated at day 35 (T)
2010-06-05 | E-GEOD-843 | biostudies-arrayexpress
Project description:The role of the transcription factor EB (TFEB) in the control of cellular functions, including in vascular bed, is mostly thought to be the regulation of lysosomal biogenesis and autophagic flux. While this is its best-known function, we report here the ability of TFEB to orchestrate a non-canonical program involved in the control of cell-cycle and VEGFR2 pathway in the developing vasculature. In endothelial cells, TFEB deletion halts proliferation by inhibiting the CDK4/Rb pathway, which regulates the cell cycle G1-S transition. In an attempt to overcome this limit, cells compensate by increasing the amount of VEGFR2 on the plasma membrane through a microRNA-mediated mechanism and the control of its membrane trafficking. TFEB transactivates the miR-15a/16-1 cluster, which limits the stability of the VEGFR2 transcript, and negatively modulates the expression of MYO1C, which regulates VEGFR2 delivery to the cell surface. In TFEB knocked-down cells, the reduced and increased amount respectively of miR-15a/16-1 and MYO1C result in the overexpression on plasmamembrane of VEGFR2, which however shows low signaling strength. Using endothelial loss-of-function Tfeb mouse mutants, we present evidence of defects in fetal and newborn mouse vasculature caused by the reduced endothelial proliferation and by the anomalous function of VEGFR2 pathway. Thus, this study revealed a new and unreported function of TFEB that expands its role beyond the regulation of autophagic pathway in the vascular system.
2018-11-20 | GSE88896 | GEO