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Vu2019 - Planarian tissue polarity

ABSTRACT: The model explores the establishment and stability of the wildtype polarity pattern in planarian flatworms. Initial conditions for A and M fields are chosen as arbitrarily perturbed to demonstrate stability of the wild type pattern. A represents the A/P polarization system, M represents the M/L polarization system and P represents the resulting superimposed and normalized polarization. P can be compared to the measured polarity data of ciliary rootlets. This simulation reproduces Figure 4C of the referenced paper. Parameter values correspond to the wild type pattern (control) as given in Table S2 of the referenced paper. The model file is in MorpheusML format and can be opened in the free, open-source multicellular modeling software Morpheus (https://morpheus.gitlab.io) to simulate the time course (movie) of the spatio-temporal dynamics.

SUBMITTER: Lutz Brusch

PROVIDER: MODEL2107170001 | BioModels | 2021-10-05

REPOSITORIES: BioModels

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Vu2019 - Planarian double-head regeneration

Project description:This spatio-temporal model explores tissue polarity re-organization during planarian double-head formation upon regeneration with beta-catenin-1 RNAi treatment. Initial conditions for A and M polarity fields are chosen near the wild type pattern and the first 100 time steps are used to establish the typical wild type splay pattern. The induction of the ectopic head occurs at time-step 100 (interpreted as tail amputation time) at the position where the former tail was (right end), subsequently affects the nearby tissue with some lag and then re-polarizes the posterior half of the tissue from time-step 200 onward. Of these polarity fields, A represents the anterior-posterior polarization system provided by the core PCP pathway, M represents the medio-lateral polarization system provided by the Ft/Ds pathway and P represents the resulting superimposed and normalized polarization. P can be compared to the observable polarity data of ciliary rootlets. This simulation reproduces Figure 4D of the referenced paper. Parameter values correspond to the beta-catenin-1(RNAi) pattern as given in Table S2 of the referenced paper. The model file is in MorpheusML format and can be opened in the free, open-source multicellular modeling software Morpheus (https://morpheus.gitlab.io) to simulate the time course (movie) of the spatio-temporal dynamics.

2021-10-06 | MODEL2110050001 | BioModels

Miyazawa2010 - changing turing patterns by spatial parameter sweep

Project description:Biologists have long been fascinated by the amazing diversity of animal colour patterns. Despite much interest, the underlying evolutionary and developmental mechanisms contributing to their rich variety remain largely unknown, especially the vivid and complex colour patterns seen in vertebrates. The model [1] shows, that complex and camouflaged animal markings can be formed by the ‘blending’ of simple colour patterns. A mathematical model predicts that crossing between animals having inverted spot patterns (for example, ‘light spots on a dark background’ and ‘ dark spots on a light background’ ) will necessarily result in hybrid offspring that have camouflaged labyrinthine patterns as ‘ blended ’ intermediate phenotypes. In [1] the authors confirmed the broad applicability of the model prediction by empirical examination of natural and artificial hybrids of salmonid fish. The results suggest an unexplored evolutionary process by means of ‘pattern blending’, as one of the possible mechanisms underlying colour pattern diversity and hybrid speciation. The model file is in MorpheusML format and can be opened in the free, open-source multicellular modeling software Morpheus (https://morpheus.gitlab.io) to simulate the time course (movie) of the spatio-temporal dynamics. It resembles figure 3a from [1], where a 2D parameter space shows the transition from black to white spots through intermediate labyrinthine patterns. 1. Miyazawa, Okamoto and Kondo, Blending of animal colour patterns by hybridization, Nature Communications, 2010

2023-09-07 | MODEL2304280001 | BioModels

Soh2020 - Spatio-temporal morphogen gradient and BMP signaling

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2021-10-06 | MODEL2012070002 | BioModels

deBack2013 - Pancreas differentiation patterning in spatio-temporal multicellular model

Project description:This model reproduces a solution (at a=1, b=20.8, eta=1e-4) of the parameter scan in Fig. 4b of the referenced paper. Equations and other parameter values are as published. Notch signaling in competition with lateral stabilization, both mediated by cell–cell interactions, can control the cell fate decision of multi-potent pancreatic progenitor cells between the exocrine and endocrine lineages and yield a scattered spatial distribution of endocrine cells, major constituents of the later islets of Langerhans. The model file is in MorpheusML format and can be opened in the free, open-source multicellular modeling software Morpheus (download from https://morpheus.gitlab.io) to simulate the time course (movie) of lineage specification in 10.000 coupled cells in the early pancreatic tissue.

2021-10-06 | MODEL2011260001 | BioModels

Mus musculus

Project description:CTCF binding polarity determines chromatin looping [4C]

| PRJNA294301 | ENA

Spatial transcriptomics reveals a conserved segment polarity program that governs muscle patterning in Nematostella vectensis

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2023-06-12 | GSE173786 | GEO

Time-resolved function of cell polarity kinases PRKCZ and PRKCI in CNS myelination [snrna_oligo]

Project description:The atypical Protein Kinase C (aPKC) is a critical component of the PAR polarity complex, as well as of cell polarity in general. There are two paralogs of aPKC in the mammalian genome. Their expression pattern and functional role in oligodendrocyte lineage differentiation and development remains heretofore uncharacterized. Here we show that both paralogs of aPKC – PRKCI, the primary transcript of Prkci and PKMz, an alternate transcript of Prkcz – are expressed during oligodendrocyte differentiation, yet are functionally non-redundant. Asymmetric cell division and early specification of the oligodendrocyte fate stage required both paralogs. By contrast, the stage of oligodendrocyte maturation involving membrane polarization and myelination of axons continued to require PKMz, but no longer needed PRKCI. Taken together, our results indicate to a two-stage role of aPKCs and cell polarity in oligodendrocyte differentiation and development.

2024-04-21 | GSE263981 | GEO

Time-resolved function of cell polarity kinases PRKCZ and PRKCI in CNS myelination [bulk_oligo]

2024-04-21 | GSE263979 | GEO

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2024-01-26 | PXD042560 | Pride

Phosphoproteomic analysis of CD2 signaling reveals an AMPK-dependent targeted granule secretion in human cytotoxic T cells

Project description:The in-depth analysis of co-stimulatory signaling enhancing the activity of cytotoxic T cells represents a major approach towards the development of immunotherapies. Here we describe that CD2 co-stimulation plays a critical role in the functioning of human cytotoxic T cells (CTLs). We found that CD2 promotes the formation of functional immune synapses by orchestrating the polarization of lytic granules towards the synaptic interface. To broadly explore the CD2 signaling network, we undertook an analysis of protein phosphorylation in CD2-stimulated CTLs, which revealed 549 unique CD2-regulated phosphorylation events in 373 proteins. CD2 stimulation elicited an intricated network of signaling events participating in the regulation of T cell metabolism, vesicular trafficking, autophagy, cell polarity and cytoskeleton organization. We further show that a functionally critical node of this network is the AMP-activated protein kinase (AMPK), which regulates granule polarization at the CTL synapse. Polarized trafficking of granules is driven by the concerted action of TAK1/LKB1/CamKK2 kinases, which locally activate AMPK enriched on CTL lysosome membranes, illustrating a novel functional cross-talk between vesicular compartments in CTLs. Our results thus establish CD2 signaling as key for regulating targeted granule secretion in CTLs and reveal an AMPK-dependent mechanism to explain how AMPK-activating drugs boost anti-tumour CTL activity.

2020-04-28 | PXD013840 | Pride

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