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
Project description:Muraro2014 - Vascular patterning in Arabidopsis roots
Using a multicellular model, maintanence of vascular patterning in Arabidopsis roots has been studied. The model that is provided here is the single-cell version of the model. The two-cell and multicellular models described in the paper can be downloaded as python scripts (follow the curation tab to get these files).
This model is described in the article:
Integration of hormonal signaling networks and mobile microRNAs is required for vascular patterning in Arabidopsis roots.
Muraro D, Mellor N, Pound MP, Help H, Lucas M, Chopard J, Byrne HM, Godin C, Hodgman TC, King JR, Pridmore TP, Helariutta Y, Bennett MJ, Bishopp A.
Proc Natl Acad Sci U S A. 2014 Jan 14;111(2):857-62.
Abstract:
As multicellular organisms grow, positional information is continually needed to regulate the pattern in which cells are arranged. In the Arabidopsis root, most cell types are organized in a radially symmetric pattern; however, a symmetry-breaking event generates bisymmetric auxin and cytokinin signaling domains in the stele. Bidirectional cross-talk between the stele and the surrounding tissues involving a mobile transcription factor, SHORT ROOT (SHR), and mobile microRNA species also determines vascular pattern, but it is currently unclear how these signals integrate. We use a multicellular model to determine a minimal set of components necessary for maintaining a stable vascular pattern. Simulations perturbing the signaling network show that, in addition to the mutually inhibitory interaction between auxin and cytokinin, signaling through SHR, microRNA165/6, and PHABULOSA is required to maintain a stable bisymmetric pattern. We have verified this prediction by observing loss of bisymmetry in shr mutants. The model reveals the importance of several features of the network, namely the mutual degradation of microRNA165/6 and PHABULOSA and the existence of an additional negative regulator of cytokinin signaling. These components form a plausible mechanism capable of patterning vascular tissues in the absence of positional inputs provided by the transport of hormones from the shoot.
This model is hosted on BioModels Database
and identified
by: BIOMD0000000522
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
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
Project description:Over time, plants have evolved flexible self-organizing patterning mechanisms to adapt tissue functionality to continuous organ growth. A clear example of this process is the multicellular organization of vascular cells into narrow and elongated conductive channels in foliar organs of Arabidopsis thaliana such as cotyledons. The establishment of a closed vascular network is achieved through the coordinated specification of newly recruited procambial cells by means of their proliferation and elongation. An important and yet poorly understood component of this process is secondary vein branching; a mechanism employed to extend vascular tissues throughout cotyledon surface. Here we revise the directionality of the formation of vascular tissues in the embryonic cotyledon of Arabidopsis and show that distal veins arise from the bifurcation of cell files contained in the midvein. Instead, proximal veins emerge from the division of provascular cells, a process partially constrained by RECEPTOR LIKE PROTEIN KINASE 2 (RPK2). Utilizing genetic, transcriptomic and live-cell imaging analyses, we show that RPK2 function is antagonized by COTYLEDON VASCULAR PATTERN 2 and its homologous CVP2 LIKE 1. Whilst RPK2 expression at the cotyledon margin prevents the branching of secondary proximal veins, the divergence of the midvein into distal veins appears to be auxin-dependent and follows a distinct regulatory mechanism. Our work supports a model in which RPK2 modulates vascular complexity independently of cell-to-cell auxin-propagation to adapt the spatial configuration of vascular tissues to organ growth.
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.