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  https://pubmed.ncbi.nlm.nih.gov/31320... Morphogenesis as Bayesian inference: A variational approach to pattern formation and control in complex biological systems Franz Kuchling, Karl Friston, Georgi Georgiev, Michael Levin (2020) Active Inference Institute information: Website: https://activeinference.org/ Twitter: https://twitter.com/InferenceActive Discord: https://discord.gg/8VNKNp4jtx YouTube: / activeinference Active Inference Livestreams: https://coda.io/@active-inference-ins... CSID: f6f0a67ae23980e5 Content Managed by ContentSafe.co

  https://pubmed.ncbi.nlm.nih.gov/31320... Morphogenesis as Bayesian inference: A variational approach to pattern formation and control in complex biological systems Franz Kuchling, Karl Friston, Georgi Georgiev, Michael Levin (2020) Active Inference Institute information: Website: https://activeinference.org/ Twitter: https://twitter.com/InferenceActive Discord: https://discord.gg/8VNKNp4jtx YouTube: / activeinference Active Inference Livestreams: https://coda.io/@active-inference-ins... CSID: f6f0a67ae23980e5 Content Managed by ContentSafe.co

  https://pubmed.ncbi.nlm.nih.gov/31320... Morphogenesis as Bayesian inference: A variational approach to pattern formation and control in complex biological systems Franz Kuchling, Karl Friston, Georgi Georgiev, Michael Levin (2020) Active Inference Institute information: Website: https://activeinference.org/ Twitter: https://twitter.com/InferenceActive Discord: https://discord.gg/8VNKNp4jtx YouTube: / activeinference Active Inference Livestreams: https://coda.io/@active-inference-ins... CSID: f6f0a67ae23980e5 Content Managed by ContentSafe.co

  https://pubmed.ncbi.nlm.nih.gov/31320... Morphogenesis as Bayesian inference: A variational approach to pattern formation and control in complex biological systems Franz Kuchling, Karl Friston, Georgi Georgiev, Michael Levin (2020) Active Inference Institute information: Website: https://activeinference.org/ Twitter: https://twitter.com/InferenceActive Discord: https://discord.gg/8VNKNp4jtx YouTube: / activeinference Active Inference Livestreams: https://coda.io/@active-inference-ins... CSID: f6f0a67ae23980e5 Content Managed by ContentSafe.co

  https://pubmed.ncbi.nlm.nih.gov/31320... Morphogenesis as Bayesian inference: A variational approach to pattern formation and control in complex biological systems Franz Kuchling, Karl Friston, Georgi Georgiev, Michael Levin (2020) Active Inference Institute information: Website: https://activeinference.org/ Twitter: https://twitter.com/InferenceActive Discord: https://discord.gg/8VNKNp4jtx YouTube: / activeinference Active Inference Livestreams: https://coda.io/@active-inference-ins... CSID: f6f0a67ae23980e5 Content Managed by ContentSafe.co

  https://pubmed.ncbi.nlm.nih.gov/31320... Morphogenesis as Bayesian inference: A variational approach to pattern formation and control in complex biological systems Franz Kuchling, Karl Friston, Georgi Georgiev, Michael Levin (2020) Second participatory discussion Active Inference Institute information: Website: https://activeinference.org/ Twitter: https://twitter.com/InferenceActive Discord: https://discord.gg/8VNKNp4jtx YouTube: / activeinference Active Inference Livestreams: https://coda.io/@active-inference-ins... CSID: 0399e56922a43e36 Content Managed by ContentSafe.co

This article is based on the Agent-action-Objective AaO-axiom and assumes that intention can be discovered and made evident. But this requirement can be satisfied only under the condition that a particular individual can be identified with his style of writing. This implies that the nature of writing becomes approachable. Getting a style under control presupposes the A-component, which is discussed with a focus on string rotation and the establishment of lawful relations that include intention in laws that are governing the patterning of strings. It is demonstrated that angular articulations are characterising dynamical string movements. However, independent of their textually embedded magnitudes, they cannot survive. As the result of the text production of two Swedish students, convoluted structures have come into existence and reflect transformations on the meaning of topological invariants. Thus, spaces have been realised, which have been shown to restrict string rotations. Over the given environments, it is demonstrated that uniqueness is achieved in the comprehension of a particular task. In the formation of motifs, the morphogenesis of intention and its structural stability have provided the basis for a 3D writing style control, while the growth curves of motifs have been shown to evolve in complex landscapes.

This article is from Development (Cambridge, England) , volume 140 . Abstract Morphogenesis of the semicircular canal ducts in the vertebrate inner ear is a dramatic example of epithelial remodelling in the embryo, and failure of normal canal development results in vestibular dysfunction. In zebrafish and Xenopus, semicircular canal ducts develop when projections of epithelium, driven by extracellular matrix production, push into the otic vesicle and fuse to form pillars. We show that in the zebrafish, extracellular matrix gene expression is high during projection outgrowth and then rapidly downregulated after fusion. Enzymatic disruption of hyaluronan in the projections leads to their collapse and a failure to form pillars: as a result, the ears swell. We have cloned a zebrafish mutant, lauscher (lau), identified by its swollen ear phenotype. The primary defect in the ear is abnormal projection outgrowth and a failure of fusion to form the semicircular canal pillars. Otic expression of extracellular matrix components is highly disrupted: several genes fail to become downregulated and remain expressed at abnormally high levels into late larval stages. The lau mutations disrupt gpr126, an adhesion class G protein-coupled receptor gene. Expression of gpr126 is similar to that of sox10, an ear and neural crest marker, and is partially dependent on sox10 activity. Fusion of canal projections and downregulation of otic versican expression in a hypomorphic lau allele can be restored by cAMP agonists. We propose that Gpr126 acts through a cAMP-mediated pathway to control the outgrowth and adhesion of canal projections in the zebrafish ear via the regulation of extracellular matrix gene expression.

This article is from Development (Cambridge, England) , volume 140 . Abstract Morphogenesis of the semicircular canal ducts in the vertebrate inner ear is a dramatic example of epithelial remodelling in the embryo, and failure of normal canal development results in vestibular dysfunction. In zebrafish and Xenopus, semicircular canal ducts develop when projections of epithelium, driven by extracellular matrix production, push into the otic vesicle and fuse to form pillars. We show that in the zebrafish, extracellular matrix gene expression is high during projection outgrowth and then rapidly downregulated after fusion. Enzymatic disruption of hyaluronan in the projections leads to their collapse and a failure to form pillars: as a result, the ears swell. We have cloned a zebrafish mutant, lauscher (lau), identified by its swollen ear phenotype. The primary defect in the ear is abnormal projection outgrowth and a failure of fusion to form the semicircular canal pillars. Otic expression of extracellular matrix components is highly disrupted: several genes fail to become downregulated and remain expressed at abnormally high levels into late larval stages. The lau mutations disrupt gpr126, an adhesion class G protein-coupled receptor gene. Expression of gpr126 is similar to that of sox10, an ear and neural crest marker, and is partially dependent on sox10 activity. Fusion of canal projections and downregulation of otic versican expression in a hypomorphic lau allele can be restored by cAMP agonists. We propose that Gpr126 acts through a cAMP-mediated pathway to control the outgrowth and adhesion of canal projections in the zebrafish ear via the regulation of extracellular matrix gene expression.

We study the effect of chemotactic signaling among mesenchymal cells. We show that the particular physiology of the mesenchymal cells allows one-dimensional collapse in contrast to the case of bacteria, and that the mesenchymal morphogenesis represents thus a more complex type of pattern formation than those found in bacterial colonies. We finally compare our theoretical predictions with recent in vitro experiments.

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In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains.

In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains.

In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains.

In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains.

In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains.

In this paper, We study an one--dimensional morphogenesis model considered by C. Stinner et al. in (Math. Meth. Appl. Sci. 2012,35 (445-465). Under homogeneous boundary conditions, we prove the existence of nonconstant positive steady states through local bifurcation theories. We also rigorously study the stability of the nonconstant solutions when the sensitivity function are chosen to be linear and logarithmic function respectively. Finally, we present numerical solutions to illustrate the formation of stable spatially inhomogeneous patterns. Our numerical simulations suggests that this model can develop very complicated and interesting structures even over one--dimensional finite domains.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This paper investigates cultural dynamics in social media by examining the proliferation and diversification of clearly-cut pieces of content: quoted texts. In line with the pioneering work of Leskovec et al. and Simmons et al. on memes dynamics we investigate in deep the transformations that quotations published online undergo during their diffusion. We deliberately put aside the structure of the social network as well as the dynamical patterns pertaining to the diffusion process to focus on the way quotations are changed, how often they are modified and how these changes shape more or less diverse families and sub-families of quotations. Following a biological metaphor, we try to understand in which way mutations can transform quotations at different scales and how mutation rates depend on various properties of the quotations.

This article is from Open Biology , volume 3 . Abstract Many organs of higher organisms are heavily branched structures and arise by an apparently similar process of branching morphogenesis. Yet the regulatory components and local interactions that have been identified differ greatly in these organs. It is an open question whether the regulatory processes work according to a common principle and how far physical and geometrical constraints determine the branching process. Here, we review the known regulatory factors and physical constraints in lung, kidney, pancreas, prostate, mammary gland and salivary gland branching morphogenesis, and describe the models that have been formulated to analyse their impacts.

This article is from PLoS Pathogens , volume 10 . Abstract Glutathione (GSH) is the most abundant cellular thiol playing an essential role in preserving a reduced cellular environment. Cellular GSH levels can be efficiently reduced by the GSH biosynthesis inhibitor, L-buthionine sulfoximine (BSO). The aim of our study was to determine the role of GSH in the growth of two C-cluster enteroviruses, poliovirus type 1 (PV1) and coxsackievirus A20 (CAV20). Our results show that the growth of both PV1 and CAV20 is strongly inhibited by BSO and can be partially reversed by the addition of GSH. BSO has no effect on viral protein synthesis or RNA replication but it strikingly reduces the accumulation of 14S pentamers in infected cells. GSH-pull down assays show that GSH directly interacts with capsid precursors and mature virus made in the absence of BSO whereas capsid precursors produced under GSH-depletion do not bind to GSH. In particular, the loss of binding of GSH may debilitate the stability of 14S pentamers, resulting in their failure to assemble into mature virus. Immunofluorescence cell imaging demonstrated that GSH-depletion did not affect the localization of viral capsid proteins to the replication complex. PV1 BSO resistant (BSOr) mutants evolved readily during passaging of the virus in the presence of BSO. Structural analyses revealed that the BSOr mutations, mapping to VP1 and VP3 capsid proteins, are primarily located at protomer/protomer interfaces. BSOr mutations might, in place of GSH, aid the stability of 14S particles that is required for virion maturation. Our observation that BSOr mutants are more heat resistant and need less GSH than wt virus to be protected from heat inactivation suggests that they possess a more stable capsid. We propose that the role of GSH during enterovirus morphogenesis is to stabilize capsid structures by direct interaction with capsid proteins both during and after the formation of mature virus particles.

This article is from PLoS Pathogens , volume 10 . Abstract Glutathione (GSH) is the most abundant cellular thiol playing an essential role in preserving a reduced cellular environment. Cellular GSH levels can be efficiently reduced by the GSH biosynthesis inhibitor, L-buthionine sulfoximine (BSO). The aim of our study was to determine the role of GSH in the growth of two C-cluster enteroviruses, poliovirus type 1 (PV1) and coxsackievirus A20 (CAV20). Our results show that the growth of both PV1 and CAV20 is strongly inhibited by BSO and can be partially reversed by the addition of GSH. BSO has no effect on viral protein synthesis or RNA replication but it strikingly reduces the accumulation of 14S pentamers in infected cells. GSH-pull down assays show that GSH directly interacts with capsid precursors and mature virus made in the absence of BSO whereas capsid precursors produced under GSH-depletion do not bind to GSH. In particular, the loss of binding of GSH may debilitate the stability of 14S pentamers, resulting in their failure to assemble into mature virus. Immunofluorescence cell imaging demonstrated that GSH-depletion did not affect the localization of viral capsid proteins to the replication complex. PV1 BSO resistant (BSOr) mutants evolved readily during passaging of the virus in the presence of BSO. Structural analyses revealed that the BSOr mutations, mapping to VP1 and VP3 capsid proteins, are primarily located at protomer/protomer interfaces. BSOr mutations might, in place of GSH, aid the stability of 14S particles that is required for virion maturation. Our observation that BSOr mutants are more heat resistant and need less GSH than wt virus to be protected from heat inactivation suggests that they possess a more stable capsid. We propose that the role of GSH during enterovirus morphogenesis is to stabilize capsid structures by direct interaction with capsid proteins both during and after the formation of mature virus particles.

This article is from PLoS Pathogens , volume 10 . Abstract Glutathione (GSH) is the most abundant cellular thiol playing an essential role in preserving a reduced cellular environment. Cellular GSH levels can be efficiently reduced by the GSH biosynthesis inhibitor, L-buthionine sulfoximine (BSO). The aim of our study was to determine the role of GSH in the growth of two C-cluster enteroviruses, poliovirus type 1 (PV1) and coxsackievirus A20 (CAV20). Our results show that the growth of both PV1 and CAV20 is strongly inhibited by BSO and can be partially reversed by the addition of GSH. BSO has no effect on viral protein synthesis or RNA replication but it strikingly reduces the accumulation of 14S pentamers in infected cells. GSH-pull down assays show that GSH directly interacts with capsid precursors and mature virus made in the absence of BSO whereas capsid precursors produced under GSH-depletion do not bind to GSH. In particular, the loss of binding of GSH may debilitate the stability of 14S pentamers, resulting in their failure to assemble into mature virus. Immunofluorescence cell imaging demonstrated that GSH-depletion did not affect the localization of viral capsid proteins to the replication complex. PV1 BSO resistant (BSOr) mutants evolved readily during passaging of the virus in the presence of BSO. Structural analyses revealed that the BSOr mutations, mapping to VP1 and VP3 capsid proteins, are primarily located at protomer/protomer interfaces. BSOr mutations might, in place of GSH, aid the stability of 14S particles that is required for virion maturation. Our observation that BSOr mutants are more heat resistant and need less GSH than wt virus to be protected from heat inactivation suggests that they possess a more stable capsid. We propose that the role of GSH during enterovirus morphogenesis is to stabilize capsid structures by direct interaction with capsid proteins both during and after the formation of mature virus particles.

By means of novel volume-diameter aspect ratio diagrams, we ponder on the current conception of crater morphogenesis analyzing crater data from beam explosions, hypervelocity collisions and drop experiments and comparing them with crater data from three moons (the Moon, Callisto, and Ganymede) and from our own experimental results. The distinctive volume-diameter scaling laws we discovered make us to conclude that simple and complex craters in satellites and planets could have been formed by granular vs. granular collisions and that central peaks and domes in complex craters were formed by a dynamic confinement of part of the impacting projectile, rather than by the uplift of the target terrain. A granulometric analysis of asteroids and central peaks and domes inside complex craters, shows boulder size distributions consistent with our hypothesis that crater internal features are the remnants of granular impactors.

By means of novel volume-diameter aspect ratio diagrams, we ponder on the current conception of crater morphogenesis analyzing crater data from beam explosions, hypervelocity collisions and drop experiments and comparing them with crater data from three moons (the Moon, Callisto, and Ganymede) and from our own experimental results. The distinctive volume-diameter scaling laws we discovered make us to conclude that simple and complex craters in satellites and planets could have been formed by granular vs. granular collisions and that central peaks and domes in complex craters were formed by a dynamic confinement of part of the impacting projectile, rather than by the uplift of the target terrain. A granulometric analysis of asteroids and central peaks and domes inside complex craters, shows boulder size distributions consistent with our hypothesis that crater internal features are the remnants of granular impactors.

By means of novel volume-diameter aspect ratio diagrams, we ponder on the current conception of crater morphogenesis analyzing crater data from beam explosions, hypervelocity collisions and drop experiments and comparing them with crater data from three moons (the Moon, Callisto, and Ganymede) and from our own experimental results. The distinctive volume-diameter scaling laws we discovered make us to conclude that simple and complex craters in satellites and planets could have been formed by granular vs. granular collisions and that central peaks and domes in complex craters were formed by a dynamic confinement of part of the impacting projectile, rather than by the uplift of the target terrain. A granulometric analysis of asteroids and central peaks and domes inside complex craters, shows boulder size distributions consistent with our hypothesis that crater internal features are the remnants of granular impactors.

This article is from PLoS Computational Biology , volume 9 . Abstract Cleft formation during submandibular salivary gland branching morphogenesis is the critical step initiating the growth and development of the complex adult organ. Previous experimental studies indicated requirements for several epithelial cellular processes, such as proliferation, migration, cell-cell adhesion, cell-extracellular matrix (matrix) adhesion, and cellular contraction in cleft formation; however, the relative contribution of each of these processes is not fully understood since it is not possible to experimentally manipulate each factor independently. We present here a comprehensive analysis of several cellular parameters regulating cleft progression during branching morphogenesis in the epithelial tissue of an early embryonic salivary gland at a local scale using an on lattice Monte-Carlo simulation model, the Glazier-Graner-Hogeweg model. We utilized measurements from time-lapse images of mouse submandibular gland organ explants to construct a temporally and spatially relevant cell-based 2D model. Our model simulates the effect of cellular proliferation, actomyosin contractility, cell-cell and cell-matrix adhesions on cleft progression, and it was used to test specific hypotheses regarding the function of these parameters in branching morphogenesis. We use innovative features capturing several aspects of cleft morphology and quantitatively analyze clefts formed during functional modification of the cellular parameters. Our simulations predict that a low epithelial mitosis rate and moderate level of actomyosin contractility in the cleft cells promote cleft progression. Raising or lowering levels of contractility and mitosis rate resulted in non-progressive clefts. We also show that lowered cell-cell adhesion in the cleft region and increased cleft cell-matrix adhesions are required for cleft progression. Using a classifier-based analysis, the relative importance of these four contributing cellular factors for effective cleft progression was determined as follows: cleft cell contractility, cleft region cell-cell adhesion strength, epithelial cell mitosis rate, and cell-matrix adhesion strength.

This article is from Reproductive Biology and Endocrinology : RB&E , volume 11 . Abstract Background: Beta-catenin (CTNNB1), as a key transcriptional regulator in the WNT signal transduction cascade, plays a pivotal role in multiple biological functions such as embryonic development and homeostasis in adults. Although it has been suggested that CTNNB1 is required for gonad development and maintenance of ovarian function in mice, little is known about the expression and functional role of CTNNB1 in gonadal development and differentiation in the chicken reproductive system. Methods: To examine sex-specific, cell-specific and temporal expression of CTNNB1 mRNA and protein during gonadal development to maturation of reproductive organs, we collected left and right gonads apart from mesonephric kidney of chicken embryos on embryonic day (E) 6, E9, E14, E18, as well as testes, oviduct and ovaries from 12-week-old and adult chickens and performed quantitative PCR, in situ hybridization, and immunohistochemical analyses. In addition, localization of Sertoli cell markers such as anti-Müllerian hormone (AMH), estrogen receptor alpha (ESR1), cyclin D1 (CCND1) and N-cadherin (CDH2) during testicular development was evaluated. Results: Results of the present study showed that CTNNB1 mRNA and protein are expressed predominantly in the seminiferous cords on E6 to E14 in the male embryonic gonad, and are mainly localized to the medullary region of female embryonic gonads from E6 to E9. In addition, CTNNB1 mRNA and protein are abundant in the Sertoli cells in the testes and expressed predominantly in luminal epithelial cells of the oviduct, but not in the ovaries from 12-week-old and adult chickens. Concomitant with CTNNB1, AMH, ESR1, CCND1 and CDH2 were detected predominantly in the seminiferous cord of the medullary region of male gonads at E9 (after sex determination) and then maintained or decreased until hatching. Interestingly, AMH, ESR1, CCND1 and CDH2 were located in seminiferous tubules of the testes from 12-weeks-old chickens and ESR1, CCND1 and CDH2 were expressed predominantly in the Sertoli cells within seminiferous tubules of adult testes. Conclusions: Collectively, these results revealed that CTNNB1 is present in gonads of both sexes during embryonic development and it may play essential roles in differentiation of Sertoli cells during formation of seminiferous tubules during development of the testes.

This article is from The Journal of Cell Biology , volume 196 . Abstract CK1-γ/gilgamesh spatially limits the planar cell polarity–regulated process of trichome formation in Drosophila through its effect on polarized vesicle recycling.

This article is from The Journal of Cell Biology , volume 198 . Abstract Apoptosis during epithelial lumen formation is mediated by hypoxia-induced expression of the proapoptotic protein Bnip3, which is promoted by AIF-mediated reactive oxygen species production and HIF-2α stabilization.

This article is from The Journal of Cell Biology , volume 198 . Abstract Apoptosis during epithelial lumen formation is mediated by hypoxia-induced expression of the proapoptotic protein Bnip3, which is promoted by AIF-mediated reactive oxygen species production and HIF-2α stabilization.

This article is from BMC Neuroscience , volume 12 . Abstract Background: The vertebrate peripheral nervous system contains sensory neurons that arise from ectodermal placodes. Placodal cells ingress to move inside the head to form sensory neurons of the cranial ganglia. To date, however, the process of placodal cell ingression and underlying cellular behavior are poorly understood as studies have relied upon static analyses on fixed tissues. Visualizing placodal cell behavior requires an ability to distinguish the surface ectoderm from the underlying mesenchyme. This necessitates high resolution imaging along the z-plane which is difficult to accomplish in whole embryos. To address this issue, we have developed an imaging system using cranial slices that allows direct visualization of placode formation. Results: We demonstrate an effective imaging assay for capturing placode development at single cell resolution using chick embryonic tissue ex vivo. This provides the first time-lapse imaging of mitoses in the trigeminal placodal ectoderm, ingression, and intercellular contacts of placodal cells. Cell divisions with varied orientations were found in the placodal ectoderm all along the apical-basal axis. Placodal cells initially have short cytoplasmic processes during ingression as young neurons and mature over time to elaborate long axonal processes in the mesenchyme. Interestingly, the time-lapse imaging data reveal that these delaminating placodal neurons begin ingression early on from within the ectoderm, where they start to move and continue on to exit as individual or strings of neurons through common openings on the basal side of the epithelium. Furthermore, dynamic intercellular contacts are abundant among the delaminating placodal neurons, between these and the already delaminated cells, as well as among cells in the forming ganglion. Conclusions: This new imaging assay provides a powerful method to analyze directly development of placode-derived sensory neurons and subsequent ganglia formation for the first time in amniotes. Viewing placode development in a head cross-section provides a vantage point from which it is possible to study comprehensive events in placode formation, from differentiation, cell ingression to ganglion assembly. Understanding how placodal neurons form may reveal a new mechanism of neurogenesis distinct from that in the central nervous system and provide new insight into how cells acquire motility from a stationary epithelial cell type.

Bibliography: p. 95-98

This article is from PLoS ONE , volume 9 . Abstract Juvenile Hormone (JH) represses metamorphosis of young instars in insects. One of the main players in hormonal signalling is Methoprene-tolerant (Met), which plays the role of JH receptor. Using the Polyneopteran insect Blattella germanica as the model and RNAi for transcript depletion, we have confirmed that Met transduces the antimetamorphic signal of JH in young nymphs and plays a role in the last nymphal instar moult in this species. Previously, the function of Met as the JH receptor had been demonstrated in the Eumetabola clade, with experiments in Holometabola (in the beetle Tribolium castaneum) and in their sister group Paraneoptera (in the bug Pyrrhocoris apterus). Our result shows that the function of Met as JH receptor is also conserved in the more basal Polyneoptera. The function of Met as JH transducer might thus predate the evolutionary innovation of metamorphosis. Moreover, expression of Met was also found in last nymphal instar of B. germanica, when JH is absent. Depletion of Met in this stage provoked deficiencies in wing growth and ecdysis problems in the imaginal moult. Down-regulation of the ecdysone-inducible gene E75A and Insulin-Like-Peptide 1 in these Met-depleted specimens suggest that Met is involved in the ecdysone and insulin signalling pathways in last nymphal instar, when JH is virtually absent.

This article is from PLoS Genetics , volume 10 . Abstract Ocular coloboma is a sight-threatening malformation caused by failure of the choroid fissure to close during morphogenesis of the eye, and is frequently associated with additional anomalies, including microphthalmia and cataracts. Although Hedgehog signaling is known to play a critical role in choroid fissure closure, genetic regulation of this pathway remains poorly understood. Here, we show that the transcription factor Sox11 is required to maintain specific levels of Hedgehog signaling during ocular development. Sox11-deficient zebrafish embryos displayed delayed and abnormal lens formation, coloboma, and a specific reduction in rod photoreceptors, all of which could be rescued by treatment with the Hedgehog pathway inhibitor cyclopamine. We further demonstrate that the elevated Hedgehog signaling in Sox11-deficient zebrafish was caused by a large increase in shha transcription; indeed, suppressing Shha expression rescued the ocular phenotypes of sox11 morphants. Conversely, over-expression of sox11 induced cyclopia, a phenotype consistent with reduced levels of Sonic hedgehog. We screened DNA samples from 79 patients with microphthalmia, anophthalmia, or coloboma (MAC) and identified two novel heterozygous SOX11 variants in individuals with coloboma. In contrast to wild type human SOX11 mRNA, mRNA containing either variant failed to rescue the lens and coloboma phenotypes of Sox11-deficient zebrafish, and both exhibited significantly reduced transactivation ability in a luciferase reporter assay. Moreover, decreased gene dosage from a segmental deletion encompassing the SOX11 locus resulted in microphthalmia and related ocular phenotypes. Therefore, our study reveals a novel role for Sox11 in controlling Hedgehog signaling, and suggests that SOX11 variants contribute to pediatric eye disorders.