title: The anterior/posterior polarity of somites is disrupted in paraxis-deficient mice.
abstract: Establishing the anterior/posterior (A/P) boundary of individual somites is important for setting up the segmental body plan of all vertebrates. Resegmentation of adjacent sclerotomes to form the vertebrae and selective migration of neural crest cells during the formation of the dorsal root ganglia and peripheral nerves occur in response to differential expression of genes in the anterior and posterior halves of the somite. Recent evidence indicates that the A/P axis is established at the anterior end of the presomitic mesoderm prior to overt somitogenesis in response to both Mesp2 and Notch signaling. Here, we report that mice deficient for paraxis, a gene required for somite epithelialization, also display defects in the axial skeleton and peripheral nerves that are consistent with a failure in A/P patterning. Expression of Mesp2 and genes in the Notch pathway were not altered in the presomitic mesoderm of paraxis(-/-) embryos. Furthermore, downstream targets of Notch activation in the presomitic mesoderm, including EphA4, were transcribed normally, indicating that paraxis was not required for Notch signaling. However, genes that were normally restricted to the posterior half of somites were present in a diffuse pattern in the paraxis(-/-) embryos, suggesting a loss of A/P polarity. Collectively, these data indicate a role for paraxis in maintaining somite polarity that is independent of Notch signaling.
authors.affiliation: Department of Biology, Arizona State University, Tempe, Arizona 85287-1501, USA.
authors.forename: J
authors.initials: J
authors.lastname: Johnson
authors.forename: J
authors.initials: J
authors.lastname: Rhee
authors.forename: S M
authors.initials: SM
authors.lastname: Parsons
authors.forename: D
authors.initials: D
authors.lastname: Brown
authors.forename: E N
authors.initials: EN
authors.lastname: Olson
authors.forename: A
authors.initials: A
authors.lastname: Rawls
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins; D019521:Body Patterning / Q000235:genetics*; D001842:Bone and Bones / Q000196:embryology; D004268:DNA-Binding Proteins / Q000235:genetics*; D036388:Ephrin-B2; D005727:Ganglia, Spinal / Q000196:embryology; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins / Q000096:biosynthesis; D008648:Mesoderm / Q000378:metabolism; D051379:Mice; D008817:Mice, Mutant Strains; D010525:Peripheral Nerves / Q000196:embryology; D051881:Receptor, Notch1; D011956:Receptors, Cell Surface; D015398:Signal Transduction; D019170:Somites; D014157:Transcription Factors / Q000096:biosynthesis; D014158:Transcription, Genetic
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D004268:DNA-Binding Proteins; D036388:Ephrin-B2; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D051881:Receptor, Notch1; D011956:Receptors, Cell Surface; D014157:Transcription Factors; C107407:Mesp2 protein, mouse; C497762:Notch1 protein, mouse; C093234:Tcf15 protein, mouse; C064045:delta protein