Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-IMG-153349

Xenbase Image ID: 153349


Fig. 1. Notch signaling promotes formation of floor plate and hypochord and represses notochord. Notch signaling was repressed by injection of mRNA encoding Su(H) DNA-binding mutant (SDBM, B, E, H, K, N) and activated by Notch intracellular domain mRNA (NICD, C, F, I, L, O). Floor plate development was assayed by expression of Netrin (A–C), F-spondin (G–I), and FoxA2 (J–L). Notochord formation was assayed by Axial protocadherin (AxPC, D–F) and Tor70 staining (brown, G–O). Tor70 staining has high variability and background, and thus should not be considered quantitative. Hypochord development was assayed by F-spondin (G–I, staining ventral to notochord) and VEGF (M–O). (A–F) Dorsal views, anterior up. (G–O) Transverse vibratome sections through middle of spinal cord at tailbud stages.

Image published in: Peyrot SM et al. (2011)

Copyright © 2011. Image reproduced with permission of the Publisher, Elsevier B. V.

GeneSynonymsSpeciesStage(s)Tissue
ntn1.Lnetrin 1, Netrin-1, ntn1l, unc-6X. laevisThroughout NF stage 17neural plate
floor plate
neural tube
pcdh1.Laxial protocadherin, axpcX. laevisThroughout NF stage 14notochord
neural plate
spon1.SF-spondinX. laevisThroughout NF stage 35 and 36hypochord
floor plate
neural tube
foxa2.LHNF-3B, hnf3-beta, hnf3b, hnf3beta, LOC108717763X. laevisThroughout NF stage 35 and 36floor plate
vegfa.Lvegf, vegf-a, vegfa-a, vegfa-bX. laevisThroughout NF stage 28hypochord

Image source: Published

Experiment + Assay Source Phenotypes and Disease
Xla Wt + dnrbpj + NF17 (in situ hybridization) fig.1.b
Expression Phenotype
decreased amount ntn1.L expression in floor plate
Xla Wt + canotch1 + NF17 (in situ hybridization) fig.1.c
Expression Phenotype
mislocalised ntn1.L expression in neural plate
increased amount ntn1.L expression in neural plate
Xla Wt + canotch1 + NF14 (in situ hybridization) fig.1.f
Expression Phenotype
decreased amount pcdh1.L expression in notochord
Xla Wt + dnrbpj + NF35/36 (in situ hybridization) fig.1.h
Expression Phenotype
decreased amount spon1.S expression in floor plate
decreased amount spon1.S expression in notochord
Xla Wt + canotch1 + NF35/36 (in situ hybridization) fig.1.i
Expression Phenotype
mislocalised pcdh1.L expression in axial mesoderm
increased amount pcdh1.L expression in axial mesoderm
Xla Wt + canotch1 + NF35/36 (immunohistochemistry) fig.1.i, l
Anatomical Phenotype
abnormal development of notochord
Xla Wt + dnrbpj + NF35/36 (in situ hybridization) fig.1.k
Expression Phenotype
decreased amount foxa2.L expression in floor plate
Xla Wt + canotch1 + NF35/36 (in situ hybridization) fig.1.l
Expression Phenotype
increased amount foxa2.L expression in axial mesoderm
Xla Wt + dnrbpj + NF28 (immunohistochemistry) fig.1.n
Anatomical Phenotype
abnormal development of hypochord
Xla Wt + dnrbpj + NF28 (in situ hybridization) fig.1.n
Expression Phenotype
decreased amount vegfa.L expression in hypochord
Xla Wt + canotch1 + NF28 (immunohistochemistry) fig.1.o
Anatomical Phenotype
abnormal development of notochord
Xla Wt + canotch1 + NF28 (in situ hybridization) fig.1.o
Expression Phenotype
mislocalised vegfa.L expression in axial mesoderm
increased amount vegfa.L expression in hypochord

Larger Image
Printer Friendly View

Return to previous page