Sonic hedgehog signaling pathway in vertebrate epithelial appendage morphogenesis: perspectives in development and evolution

Chuong, Cheng Ming; Patel, Nila; Lin, Jeen‐Shang; Jung, Han‐Sung; Widelitz, Randall B.

doi:10.1007/pl00000650

Cited by 104 publications

(81 citation statements)

References 62 publications

(66 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These data extend previously documented roles for hedgehog signaling in dermal bone development (29,30) and suggest that this pathway plays an important role in polarizing dermal bone development along a proximal-distal axis. It is well established that hedgehog signaling is critical for the proper patterning and polarization of several organs in various animal taxa (32)(33)(34)(35)(36)(37), but here a similar role has been documented for bone development. The extent to which hedgehog-mediated outgrowth of other dermal bones (e.g., RA) has influenced species-specific differences in craniofacial shape would be a fruitful area of future investigation.…”

Section: Manipulation Of Hedgehog Pathway Signaling Affects Bone Devementioning

confidence: 75%

Craniofacial divergence and ongoing adaptation via the hedgehog pathway

Roberts

Albertson

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

114

148

View full text Add to dashboard Cite

Adaptive variation in craniofacial structure contributes to resource specialization and speciation, but the genetic loci that underlie craniofacial adaptation remain unknown. Here we show that alleles of the hedgehog pathway receptor Patched1 (Ptch1) gene are responsible for adaptive variation in the shape of the lower jaw both within and among genera of Lake Malawi cichlid fish. The evolutionarily derived allele of Ptch1 reduces the length of the retroarticular (RA) process of the lower jaw, a change predicted to increase speed of jaw rotation for improved suction-feeding. The alternate allele is associated with a longer RA and a more robustly mineralized jaw, typical of species that use a biting mode of feeding. Genera with the most divergent feeding morphologies are nearly fixed for different Ptch1 alleles, whereas species with intermediate morphologies still segregate variation at Ptch1. Thus, the same alleles that help to define macroevolutionary divergence among genera also contribute to microevolutionary fine-tuning of adaptive traits within some species. Variability of craniofacial morphology mediated by Ptch1 polymorphism has likely contributed to niche partitioning and ecological speciation of these fishes.T he astounding diversity of vertebrate craniofacial morphology reflects adaptation to a wide variety of resources and environments. Evolution of craniofacial structure has been key to niche specialization and speciation in vertebrates (1), most famously exemplified by the varied beak morphology of Darwin's finches (2). The radiation of finches demonstrates both speciesdefining craniofacial divergence (2) and rapid adaptation of craniofacial morphology within species over the course of a few years in response to changes in resource availability (3). Although shifts in the expression of key craniofacial genes have been correlated with differences in trophic morphology among species of birds and cichlid fishes (4-8), the specific genetic loci producing these differences remain uncharacterized. As a result, it is not clear whether interspecific divergence and intraspecific adaptation share the same molecular genetic basis.

show abstract

Section: Manipulation Of Hedgehog Pathway Signaling Affects Bone Devementioning

confidence: 75%

Craniofacial divergence and ongoing adaptation via the hedgehog pathway

Roberts

Albertson

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

114

148

View full text Add to dashboard Cite

show abstract

“…JAG1 and DLL1 participate in the notch signaling pathway, which affects the implementation of differentiation, proliferation, and apoptotic programs, providing a general developmental tool to influence organ formation and morphogenesis (6,52). In addition, IPA revealed that copper could significantly modulate sonic hedgehog signaling, which is critical in vertebrate development (14). These results suggest that the modulation of notch and sonic hedgehog signaling may be components of molecular mechanisms underlying copper-induced developmental abnormalities.…”

Section: Continuedmentioning

confidence: 83%

“…There were also enriched GO categories that mapped to specific treatment conditions: oxygen and ROS metabolism and IGF binding (400 M, 8 h); ubiquitin-protein ligase activity (600 M, 8 h); endosome organization and (2) Lipid transport (8)* Cholesterol binding (2) Lipoprotein metabolism (6)* Cholesterol metabolism (4) Acyl-CoA binding (3) Hemoglobin binding (2) Alcohol metabolism (19) Platelet activation (2) Amine metabolism (26) Regulation of body fluids (4) Chromatin assembly (6) Serine-type endopeptidase inhibitor activity (5) Creatine biosynthesis (2) Wound healing (4) Deoxyribonucleotide biosynthesis ( (2) B cell-mediated immunity (7) Hemoglobin binding (2) Complement activation (7) Lipid binding (9) Creatine biosynthesis (2) Cytolysis (4) Hormone metabolism (10) Lipid transporter activity (13) Nickel ion binding (2) Oxidoreductase activity (52) Positive regulation of immune response (7) Serine-type peptidase activity (14) Xenobiotic metabolism (5) Shown are Gene Ontology (GO) categories with P Յ 0.005. Responsive genes were 2-fold downregulated with FDR P Յ 0.05.…”

Section: Go Analysis Of Differentially Expressed Genesmentioning

confidence: 99%

Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper

Song

Freedman

2009

Physiological Genomics

View full text Add to dashboard Cite

Copper is an essential trace element; however, at supraphysiological levels, it can be extremely toxic. Microarray data from HepG2 cells exposed to 100, 200, 400, and 600 μM copper for 4, 8, 12 and 24 h were generated and analyzed. Principal components, K-means, and hierarchical clustering, interactome, and pathway mapping analyses indicated that these exposure conditions induce physiological and toxicological changes in the HepG2 transcriptome. As a general trend, when the level of toxicity increases, the number and diversity of affected genes, Gene Ontology categories, regulatory pathways, and complexity of interactomes increase. Physiological responses to copper include transition metal ion binding and responses to stress/stimulus, whereas toxicological responses include apoptosis, morphogenesis, and negative regulation of biomolecule metabolism. The global gene expression profile was overlaid onto biomolecular interaction networks and signal transduction cascades using pathway mapping and interactome identification. This analysis indicated that copper modulates signal transduction pathways associated with MAPK, NF-κB, death receptor, IGF-I, hypoxia, IL-10, IL-2, IL-6, EGF, Toll-like receptor, protein ubiquitination, xenobiotic metabolism, leukocyte extravasation, complement and coagulation, and sonic hedgehog signaling. These results provide insights into the global and molecular mechanisms regulating the physiological and toxicological responses to metal exposure.

show abstract

“…Quantitation of these complex elements of tissue pattern is essential to establish a ruler against which to accurately compare perturbances in the system. The intestinal mesenchymal clusters have several similarities to the mesenchymal condensates involved in the patterning of hair, teeth, tongue papillae, feathers, and hair follicles (13,26,(33)(34)(35)(36)(37)(38)(39). Like the dermal condensates associated with feather formation in the chick, villus clusters first arise in anterior and dorsal midline regions and then spread posteriorly and laterally (33).…”

Section: Discussionmentioning

confidence: 99%

Hedgehog-responsive mesenchymal clusters direct patterning and emergence of intestinal villi

Walton

Kolterud

Czerwinski

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

144

230

View full text Add to dashboard Cite

In the adult intestine, an organized array of finger-like projections, called villi, provide an enormous epithelial surface area for absorptive function. Villi first emerge at embryonic day (E) 14.5 from a previously flat luminal surface. Here, we analyze the cell biology of villus formation and examine the role of paracrine epithelial Hedgehog (Hh) signals in this process. We find that, before villus emergence, tight clusters of Hh-responsive mesenchymal cells form just beneath the epithelium. Cluster formation is dynamic; clusters first form dorsally and anteriorly and spread circumferentially and posteriorly. Statistical analysis of cluster distribution reveals a patterned array; with time, new clusters form in spaces between existing clusters, promoting approximately four rounds of villus emergence by E18.5. Cells within mesenchymal clusters express Patched1 and Gli1, as well as Pdgfrα, a receptor previously shown to participate in villus development. BrdU-labeling experiments show that clusters form by migration and aggregation of Hh-responsive cells. Inhibition of Hh signaling prevents cluster formation and villus development, but does not prevent emergence of villi in areas where clusters have already formed. Conversely, increasing Hh signaling increases the size of villus clusters and results in exceptionally wide villi. We conclude that Hh signals dictate the initial aspects of the formation of each villus by controlling mesenchymal cluster aggregation and regulating cluster size.epithelial-mesenchymal cross-talk | field pattern | villus morphogenesis

show abstract

Sonic hedgehog signaling pathway in vertebrate epithelial appendage morphogenesis: perspectives in development and evolution

Cited by 104 publications

References 62 publications

Craniofacial divergence and ongoing adaptation via the hedgehog pathway

Craniofacial divergence and ongoing adaptation via the hedgehog pathway

Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper

Hedgehog-responsive mesenchymal clusters direct patterning and emergence of intestinal villi

Contact Info

Product

Resources

About