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.
Search Criteria
Gene/CloneSpeciesStageAnatomy ItemExperimenter
six1xenopus   

Too many results?Too few results?

Experiment details for six1

Adams DS et al. (2016) Assay

Bioelectric signalling via potassium channels: a mechanism for craniofacial dysmorphogenesis in KCNJ2-associated Andersen-Tawil Syndrome.

Gene Clone Species Stages Anatomy
six1.L laevis NF stage 18 to NF stage 21 neural crest , otic placode , neural fold
six1.L laevis NF stage 28 otic vesicle , lens , forebrain , hyoid crest , branchial crest , [+]

Display additional annotations [+]
  Fig. S3. WISH for craniofacial patterning genes in embryos injected with the dominant negative (DN) D71V mRNA and with WT KCNJ2. Ten markers were used to characterize the effect of the DN and WT KCNJ2s on craniofacial patterning. The marker is indicated to the left of each row; two columns of images each are presented for untreated controls (No Treatment), embryos injected with the D71V DN variant, and embryos injected with the WT KCNJ2 construct. The normal pattern, at two different stages, is shown in the two left most columns. Examples of mispatterning of the markers are shown in the other columns. There was no consistent difference between the effects of the DN and the WT, indicating that the direction of change of Vmem does not prescribe a particular subset of defects.

Gene Clone Species Stages Anatomy
six1.L laevis NF stage 19 to NF stage 21 olfactory placode , otic placode , lens placode , neural plate , neural fold

Display additional annotations [+]
  Figure 7. Whole-mount ISH for well-known markers of craniofacial development in embryos injected with mRNA encoding D71V. Shown is a subset of the WISHs performed (see also Supplementary Fig. S3). This set represents at least two markers each of the relevant tissues, i.e. neural crest and the three placodes studied. A, chart showing locations of marker expression. B, normal (1st column), over-expressed (2nd column) and under-expressed (3rd column) examples from each of five representative markers. Red arrows point to positions of abnormal signal patterns; the green arrow in v points to normal expression on the side opposite the disrupted pattern. The patterns we saw, even in injected embryos that did not have significantly more misexpression than background, are consistent with incorrect or incomplete differentiation (ii, iii, v, vi, viii, ix) and anomalies in neural crest migration (xi, xii, xiv, xv). To date, we have not detected any correlation between the types or magnitudes of disruptions caused and the identity of the ion flux-perturbing construct injected.