Microdissection data of 3 vascular bundles stages - Brachypodium Vascular ontogeny
Ontology highlight
ABSTRACT:
ORGANISM(S): Brachypodium distachyon
PROVIDER: GSE162395 | GEO | 2021/04/28
REPOSITORIES: GEO
Similar Datasets
Project description:microdissection data of 3 vascular bundles stages - Brachypodium Vascular ontogeny
| PRJNA681783 | ENA
Project description:The molecular mechanisms that control the ordered patterning of vascular tissue development in plant are not well understood. Several models propose a two component for plant vascular differentiation in which requires both an inducer of vascular tissue an also an inhibitory component that prevents the formation of vascular bundles near pre-existing bundles by a process often termed lateral inhibition. We have identified two recessive allelic mutants in Arabidopsis, designated continuous vascular (cov-1, cov-2), which display a dramatic increase in vascular tissue in the stem in place of the interfascicular region that normally separates the vascular bundles. The mutant plants exhibited normal vascular patterning in leaves and cotyledons. Analysis of the interaction of cov with known auxin signalling mutant and direct analysis of auxin concentrations suggests that cov affects vascular pattering by some mechanism that is independent of auxin. COV is expressed in all plant tissue but more highly in developing flowers and stems. The COV protein is predicted to be an integral membrane protein of unknown function, conserved in both plants and bacteria that is involved in negatively regulating the differentiation of the vascular tissue in the stem of Arabidopsis.The phenotype of COV exhibits some similarities to acl5 which is known to be a defect in the gene for spermidine synthase. Consequently, we are interested to test the idea that COV may be involved in the transport or perception of polyamines and that polyamines may be essential signals in normal vascular tissue development. Clearly, it this proves to be the case we would expect to see some differences in the transcript levels of genes associated with these pathways. Experimenter name = Simon Turner; Experimenter phone = 0161 275 5751; Experimenter fax = 0161 275 3938; Experimenter address = University of Manchester; Experimenter address = School of Biological Sciences; Experimenter address = 3.614 Stopford building; Experimenter address = Oxford Rd; Experimenter address = Manchester; Experimenter zip/postal_code = M13 9PT; Experimenter country = UK Experiment Overall Design: 8 samples were used in this experiment
2008-06-14 | E-GEOD-5729 | biostudies-arrayexpress
Project description:The molecular mechanisms that control the ordered patterning of vascular tissue development in plant are not well understood. Several models propose a two component for plant vascular differentiation in which requires both an inducer of vascular tissue an also an inhibitory component that prevents the formation of vascular bundles near pre-existing bundles by a process often termed lateral inhibition. We have identified two recessive allelic mutants in Arabidopsis, designated continuous vascular (cov-1, cov-2), which display a dramatic increase in vascular tissue in the stem in place of the interfascicular region that normally separates the vascular bundles. The mutant plants exhibited normal vascular patterning in leaves and cotyledons. Analysis of the interaction of cov with known auxin signalling mutant and direct analysis of auxin concentrations suggests that cov affects vascular pattering by some mechanism that is independent of auxin. COV is expressed in all plant tissue but more highly in developing flowers and stems. The COV protein is predicted to be an integral membrane protein of unknown function, conserved in both plants and bacteria that is involved in negatively regulating the differentiation of the vascular tissue in the stem of Arabidopsis.The phenotype of COV exhibits some similarities to acl5 which is known to be a defect in the gene for spermidine synthase. Consequently, we are interested to test the idea that COV may be involved in the transport or perception of polyamines and that polyamines may be essential signals in normal vascular tissue development. Clearly, it this proves to be the case we would expect to see some differences in the transcript levels of genes associated with these pathways. Experimenter name = Simon Turner Experimenter phone = 0161 275 5751 Experimenter fax = 0161 275 3938 Experimenter address = University of Manchester Experimenter address = School of Biological Sciences Experimenter address = 3.614 Stopford building Experimenter address = Oxford Rd Experimenter address = Manchester Experimenter zip/postal_code = M13 9PT Experimenter country = UK Keywords: genetic_modification_design
2007-01-08 | GSE5729 | GEO
Project description:Arabidopsis CLE41 regulates vascular organisation, cell division and xylem differentiation. 35S::CLE41 lines are characterised by an increase in the number of undifferentiated cells in vascular bundles and by radial patterning defects. To identify further genetic components involved in controlling vascular development, we compared the transcriptomes of one 35S::CLE41 line with that of wild type counterparts using microarray analysis. Inflorescence stem tissue was compared in 5 weeks old plants 1 cm above the rosette leaves where vascular bundles of 35S::CLE41 plants contained an average of 100.7 ± 9.1 undifferentiated cells compared to 59.5 ± 5.5 in wild type counterparts. Genes with a putative role in vascular development demonstrate changes in gene expression between the two genotypes tested.
2018-12-01 | GSE123162 | GEO
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
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:Changes of gene expression in primary cell cultures of salmon adipose-derived stromal-vascular fraction were studied at six time-points that covered the key differentiation events: confluence, clonal expansion, determination and establishment of the mature adipocyte phenotype. Time-course experiment: six developmental stages of stromal-vascular fraction against the pooled reference. Biological replicates: 5 per developmental stage, pooled samples of all 6 stages were used as common reference. One stage per array.
2010-10-08 | E-GEOD-18389 | biostudies-arrayexpress
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: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.
2020-01-01 | GSE139323 | GEO
Project description:The molecular mechanisms guiding oriented cell divisions in the root vascular tissues of Arabidopsis thaliana are still poorly characterized. By overlapping bulk and single-cell transcriptomic datasets, we unveiled TETRASPANIN1 (TET1) as a putative regulator in this process. TET1 is expressed in root vascular cells and loss-of-function mutants contain fewer vascular cells files. We further generated and characterized a CRISPR deletion mutant and show, unlike previously described mutants, that the full knock out is additionally missing endodermal cells in a stochastic way. Finally, we show that HA-tagged versions of TET1 are functional in contrast to fluorescent TET1 translational fusions. Immunostaining using HA-TET1 lines complementing the mutant phenotype suggested a dual plasma membrane and intracellular localization in the root vasculature and a polar membrane localization in young cortex, endodermal and initial cells. Taken together, we show that TET1 is involved in both vascular proliferation and ground tissue patterning. Our initial results pave the way for future work into deciphering its precise mode of action.
2024-01-11 | GSE244902 | GEO