Other search tools

About this data

The publication data currently available has been vetted by Vanderbilt faculty, staff, administrators and trainees. The data itself is retrieved directly from NCBI's PubMed and is automatically updated on a weekly basis to ensure accuracy and completeness.

If you have any questions or comments, please contact us.

Results: 1 to 10 of 152

Publication Record

Connections

Spatiotemporal Control of Morphogen Delivery to Pattern Stem Cell Differentiation in Three-Dimensional Hydrogels.
O'Grady BJ, Balikov DA, Lippmann ES, Bellan LM
(2019) Curr Protoc Stem Cell Biol 51: e97
MeSH Terms: Cell Differentiation, Cells, Cultured, Hydrogels, Morphogenesis, Stem Cells, Tissue Engineering
Show Abstract · Added March 18, 2020
Morphogens are biological molecules that alter cellular identity and behavior across both space and time. During embryonic development, morphogen spatial localization can be confined to small volumes in a single tissue or permeate throughout an entire organism, and the temporal effects of morphogens can range from fractions of a second to several days. In most cases, morphogens are presented as a gradient to adjacent cells within tissues to pattern cell fate. As such, to appropriately model development and build representative multicellular architectures in vitro, it is vital to recapitulate these gradients during stem cell differentiation. However, the ability to control morphogen presentation within in vitro systems remains challenging. Here, we describe an innovative platform using channels patterned within thick, three-dimensional hydrogels that deliver multiple morphogens to embedded cells, thereby demonstrating exquisite control over both spatial and temporal variations in morphogen presentation. This generalizable approach should have broad utility for researchers interested in patterning in vitro tissue structures. © 2019 by John Wiley & Sons, Inc.
© 2019 John Wiley & Sons, Inc.
0 Communities
1 Members
0 Resources
6 MeSH Terms
Mechanisms that regulate morphogenesis of a highly branched neuron in C. elegans.
Sundararajan L, Stern J, Miller DM
(2019) Dev Biol 451: 53-67
MeSH Terms: Animals, Axons, Caenorhabditis elegans, Dendrites, Morphogenesis, Sensory Receptor Cells
Show Abstract · Added March 3, 2020
The shape of an individual neuron is linked to its function with axons sending signals to other cells and dendrites receiving them. Although much is known of the mechanisms for axonal outgrowth, the striking complexity of dendritic architecture has hindered efforts to uncover pathways that direct dendritic branching. Here we review the results of an experimental strategy that exploits the power of genetic analysis and live cell imaging of the PVD sensory neuron in C. elegans to reveal key molecular drivers of dendrite morphogenesis.
Copyright © 2019. Published by Elsevier Inc.
0 Communities
1 Members
0 Resources
MeSH Terms
Regulation of the Pancreatic Exocrine Differentiation Program and Morphogenesis by Onecut 1/Hnf6.
Kropp PA, Zhu X, Gannon M
(2019) Cell Mol Gastroenterol Hepatol 7: 841-856
MeSH Terms: Acinar Cells, Animals, Animals, Newborn, Base Sequence, Cell Differentiation, Cell Proliferation, Embryo, Mammalian, Epithelium, Gene Expression Regulation, Developmental, Hepatocyte Nuclear Factor 6, Mice, Morphogenesis, Pancreas, Exocrine
Show Abstract · Added March 29, 2019
BACKGROUND & AIMS - The Onecut 1 transcription factor (Oc1, a.k.a. HNF6) promotes differentiation of endocrine and duct cells of the pancreas; however, it has no known role in acinar cell differentiation. We sought to better understand the role of Oc1 in exocrine pancreas development and to identify its direct transcriptional targets.
METHODS - Pancreata from Oc1 (Oc1;Pdx1-Cre) mouse embryos and neonates were analyzed morphologically. High-throughput RNA-sequencing was performed on control and Oc1-deficient pancreas; chromatin immunoprecipitation sequencing was performed on wild-type embryonic mouse pancreata to identify direct Oc1 transcriptional targets. Immunofluorescence labeling was used to confirm the RNA-sequencing /chromatin immunoprecipitation sequencing results and to further investigate the effects of Oc1 loss on acinar cells.
RESULTS - Loss of Oc1 from the developing pancreatic epithelium resulted in disrupted duct and acinar cell development. RNA-sequencing revealed decreased expression of acinar cell regulatory factors (Nr5a2, Ptf1a, Gata4, Mist1) and functional genes (Amylase, Cpa1, Prss1, Spink1) at embryonic day (e) 18.5 in Oc1 samples. Approximately 1000 of the altered genes were also identified as direct Oc1 targets by chromatin immunoprecipitation sequencing, including most of the previously noted genes. By immunolabeling, we confirmed that Amylase, Mist1, and GATA4 protein levels are significantly decreased by P2, and Spink1 protein levels were significantly reduced and mislocalized. The pancreatic duct regulatory factors Hnf1β and FoxA2 were also identified as direct Oc1 targets.
CONCLUSIONS - These findings confirm that Oc1 is an important regulator of both duct and acinar cell development in the embryonic pancreas. Novel transcriptional targets of Oc1 have now been identified and provide clarity into the mechanisms of Oc1 transcriptional regulation in the developing exocrine pancreas. Oc1 can now be included in the gene-regulatory network of acinar cell regulatory genes. Oc1 regulates other acinar cell regulatory factors and acinar cell functional genes directly, and it can also regulate some acinar cell regulatory factors (eg, Mist1) indirectly. Oc1 therefore plays an important role in acinar cell development.
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
1 Communities
1 Members
0 Resources
13 MeSH Terms
Spatiotemporal control and modeling of morphogen delivery to induce gradient patterning of stem cell differentiation using fluidic channels.
O'Grady B, Balikov DA, Wang JX, Neal EK, Ou YC, Bardhan R, Lippmann ES, Bellan LM
(2019) Biomater Sci 7: 1358-1371
MeSH Terms: Cell Differentiation, Cells, Cultured, Humans, Microfluidic Analytical Techniques, Models, Biological, Morphogenesis, Stem Cells
Show Abstract · Added March 18, 2020
The process of cell differentiation in a developing embryo is influenced by numerous factors, including various biological molecules whose presentation varies dramatically over space and time. These morphogens regulate cell fate based on concentration profiles, thus creating discrete populations of cells and ultimately generating large, complex tissues and organs. Recently, several in vitro platforms have attempted to recapitulate the complex presentation of extrinsic signals found in nature. However, it has been a challenge to design versatile platforms that can dynamically control morphogen gradients over extended periods of time. To address some of these issues, we introduce a platform using channels patterned in hydrogels to deliver multiple morphogens to cells in a 3D scaffold, thus creating a spectrum of cell phenotypes based on the resultant morphogen gradients. The diffusion coefficient of a common small molecule morphogen, retinoic acid (RA), was measured within our hydrogel platform using Raman spectroscopy and its diffusion in our platform's geometry was modeled using finite element analysis. The predictive model of spatial gradients was validated in a cell-free hydrogel, and temporal control of morphogen gradients was then demonstrated using a reporter cell line that expresses green fluorescent protein in the presence of RA. Finally, the utility of this approach for regulating cell phenotype was demonstrated by generating opposing morphogen gradients to create a spectrum of mesenchymal stem cell differentiation states.
0 Communities
1 Members
0 Resources
MeSH Terms
The Elegance of Sonic Hedgehog: Emerging Novel Functions for a Classic Morphogen.
Garcia ADR, Han YG, Triplett JW, Farmer WT, Harwell CC, Ihrie RA
(2018) J Neurosci 38: 9338-9345
MeSH Terms: Animals, Hedgehog Proteins, Humans, Morphogenesis, Neural Stem Cells, Signal Transduction, Synapses
Show Abstract · Added April 10, 2019
Sonic Hedgehog (SHH) signaling has been most widely known for its role in specifying region and cell-type identity during embryonic morphogenesis. This mini-review accompanies a 2018 SFN mini-symposium that addresses an emerging body of research focused on understanding the diverse roles for Shh signaling in a wide range of contexts in neurodevelopment and, more recently, in the mature CNS. Such research shows that Shh affects the function of brain circuits, including the production and maintenance of diverse cell types and the establishment of wiring specificity. Here, we review these novel and unexpected functions and the unanswered questions regarding the role of SHH and its signaling pathway members in these cases.
Copyright © 2018 the authors 0270-6474/18/389338-08$15.00/0.
0 Communities
1 Members
0 Resources
7 MeSH Terms
A Dendritic Guidance Receptor Complex Brings Together Distinct Actin Regulators to Drive Efficient F-Actin Assembly and Branching.
Zou W, Dong X, Broederdorf TR, Shen A, Kramer DA, Shi R, Liang X, Miller DM, Xiang YK, Yasuda R, Chen B, Shen K
(2018) Dev Cell 45: 362-375.e3
MeSH Terms: Actin Cytoskeleton, Animals, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Cell Membrane, Dendrites, Membrane Proteins, Morphogenesis, Neurogenesis, Sensory Receptor Cells, Signal Transduction
Show Abstract · Added March 26, 2019
Proper morphogenesis of dendrites plays a fundamental role in the establishment of neural circuits. The molecular mechanism by which dendrites grow highly complex branches is not well understood. Here, using the Caenorhabditis elegans PVD neuron, we demonstrate that high-order dendritic branching requires actin polymerization driven by coordinated interactions between two membrane proteins, DMA-1 and HPO-30, with their cytoplasmic interactors, the RacGEF TIAM-1 and the actin nucleation promotion factor WAVE regulatory complex (WRC). The dendrite branching receptor DMA-1 directly binds to the PDZ domain of TIAM-1, while the claudin-like protein HPO-30 directly interacts with the WRC. On dendrites, DMA-1 and HPO-30 form a receptor-associated signaling complex to bring TIAM-1 and the WRC to close proximity, leading to elevated assembly of F-actin needed to drive high-order dendrite branching. The synergistic activation of F-actin assembly by scaffolding distinct actin regulators might represent a general mechanism in promoting complex dendrite arborization.
Copyright © 2018. Published by Elsevier Inc.
0 Communities
1 Members
0 Resources
MeSH Terms
Tuning Hsf1 levels drives distinct fungal morphogenetic programs with depletion impairing Hsp90 function and overexpression expanding the target space.
Veri AO, Miao Z, Shapiro RS, Tebbji F, O'Meara TR, Kim SH, Colazo J, Tan K, Vyas VK, Whiteway M, Robbins N, Wong KH, Cowen LE
(2018) PLoS Genet 14: e1007270
MeSH Terms: Blotting, Western, Candida albicans, Chromatin Immunoprecipitation, Genes, Fungal, HSP90 Heat-Shock Proteins, Heat Shock Transcription Factors, Morphogenesis, Oligonucleotide Array Sequence Analysis, Reverse Transcriptase Polymerase Chain Reaction, Sequence Analysis, RNA, Temperature, Virulence
Show Abstract · Added November 7, 2019
The capacity to respond to temperature fluctuations is critical for microorganisms to survive within mammalian hosts, and temperature modulates virulence traits of diverse pathogens. One key temperature-dependent virulence trait of the fungal pathogen Candida albicans is its ability to transition from yeast to filamentous growth, which is induced by environmental cues at host physiological temperature. A key regulator of temperature-dependent morphogenesis is the molecular chaperone Hsp90, which has complex functional relationships with the transcription factor Hsf1. Although Hsf1 controls global transcriptional remodeling in response to heat shock, its impact on morphogenesis remains unknown. Here, we establish an intriguing paradigm whereby overexpression or depletion of C. albicans HSF1 induces morphogenesis in the absence of external cues. HSF1 depletion compromises Hsp90 function, thereby driving filamentation. HSF1 overexpression does not impact Hsp90 function, but rather induces a dose-dependent expansion of Hsf1 direct targets that drives overexpression of positive regulators of filamentation, including Brg1 and Ume6, thereby bypassing the requirement for elevated temperature during morphogenesis. This work provides new insight into Hsf1-mediated environmentally contingent transcriptional control, implicates Hsf1 in regulation of a key virulence trait, and highlights fascinating biology whereby either overexpression or depletion of a single cellular regulator induces a profound developmental transition.
0 Communities
1 Members
0 Resources
MeSH Terms
Neuronal Fat and Dendrite Morphogenesis: The Goldilocks Effect.
Sundararajan L, Miller DM
(2018) Trends Neurosci 41: 250-252
MeSH Terms: Animals, Dendrites, Drosophila, Drosophila Proteins, Larva, Morphogenesis, Neurogenesis
Show Abstract · Added March 26, 2019
Two recent studies by Meltzer et al. and Ziegler et al. use Drosophila larvae to demonstrate that cell-autonomous regulation of lipid biosynthesis defines the complexity and function of highly branched nociceptive neurons. Their findings show that lipid biosynthesis in the neuron is fine-tuned for optimal dendrite morphology and sensitivity.
Copyright © 2018 Elsevier Ltd. All rights reserved.
0 Communities
1 Members
0 Resources
MeSH Terms
Apical polarization and lumenogenesis: The apicosome sheds new light.
Romero-Morales AI, Ortolano NA, Gama V
(2017) J Cell Biol 216: 3891-3893
MeSH Terms: Germ Layers, Humans, Morphogenesis, Pluripotent Stem Cells
Show Abstract · Added March 14, 2018
Establishment of apico-basal polarity is critical for the lumenal epiblast-like morphogenesis of human pluripotent stem cells (hPSCs). In this issue, Taniguchi et al. (2017. https://doi.org/10.1083.jcb201704085) describe a structure called the apicosome, generated in single hPSCs, that allows them to self-organize and form the lumenal epiblast-like stage.
© 2017 Romero-Morales et al.
0 Communities
1 Members
0 Resources
4 MeSH Terms
RHOA GTPase Controls YAP-Mediated EREG Signaling in Small Intestinal Stem Cell Maintenance.
Liu M, Zhang Z, Sampson L, Zhou X, Nalapareddy K, Feng Y, Akunuru S, Melendez J, Davis AK, Bi F, Geiger H, Xin M, Zheng Y
(2017) Stem Cell Reports 9: 1961-1975
MeSH Terms: Adaptor Proteins, Signal Transducing, Animals, Cell Cycle Proteins, Cell Differentiation, Cell Proliferation, Epiregulin, Epithelium, Gene Expression Regulation, Developmental, Intestine, Small, Mice, Mice, Knockout, Morphogenesis, Phosphoproteins, Stem Cells, Wnt Signaling Pathway, beta Catenin, rho GTP-Binding Proteins
Show Abstract · Added February 7, 2018
RHOA, a founding member of the Rho GTPase family, is critical for actomyosin dynamics, polarity, and morphogenesis in response to developmental cues, mechanical stress, and inflammation. In murine small intestinal epithelium, inducible RHOA deletion causes a loss of epithelial polarity, with disrupted villi and crypt organization. In the intestinal crypts, RHOA deficiency results in reduced cell proliferation, increased apoptosis, and a loss of intestinal stem cells (ISCs) that mimic effects of radiation damage. Mechanistically, RHOA loss reduces YAP signaling of the Hippo pathway and affects YAP effector epiregulin (EREG) expression in the crypts. Expression of an active YAP (S112A) mutant rescues ISC marker expression, ISC regeneration, and ISC-associated Wnt signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP in RHOA-regulated ISC function. EREG treatment or active β-catenin Catnb mutant expression rescues the RhoA KO ISC phenotypes. Thus, RHOA controls YAP-EREG signaling to regulate intestinal homeostasis and ISC regeneration.
Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
0 Communities
1 Members
0 Resources
17 MeSH Terms