ZFIN ID: ZDB-FIG-210113-11
Danesin et al., 2021 - Sulf2a controls Shh-dependent neural fate specification in the developing spinal cord. Scientific Reports   11:118 Full text @ Sci. Rep.
ADDITIONAL FIGURES
PHENOTYPE:
Fish:
Knockdown Reagents:
Observed In:
Stage: Long-pec

Figure 3

Sulf2a depletion impairs OPC development. Side views of 48 hpf embryos. (a-f) Detection (a–e) and quantification (f) of OPCs by immunodetection of Sox10 (green in a–c, red in d,e) in Tg(olig2:DsRed) embryos (red in a–c) injected with ctrlMO (a, n = 73), sulf2aMOATG (b, n = 31) or sulf2aMOsplice (c, n = 47) and wild-type (d, n = 10) or sulf2a−/− (e, n = 48) Tg(olig2:GFP) embryos (green in d,e) from 9 and 6 independent experiments, respectively. Datasets were compared with Mann Whitney’s test (two-tailed). Data are presented as mean number of cells per embryo ± s.d (*p < 0.05, ****p < 0.0001).

Gene Expression Details No data available
Antibody Labeling Details No data available
Phenotype Details
Fish Conditions Stage Phenotype
sulf2aups9/ups9; vu12Tg standard conditions Long-pec oligodendrocyte cell fate specification decreased occurrence, abnormal
Long-pec spinal cord oligodendrocyte decreased amount, abnormal
vu19Tg + MO1-sulf2a standard conditions Long-pec oligodendrocyte cell fate specification decreased occurrence, abnormal
Long-pec spinal cord oligodendrocyte decreased amount, abnormal
vu19Tg + MO3-sulf2a standard conditions Long-pec oligodendrocyte cell fate specification decreased occurrence, abnormal
Long-pec spinal cord oligodendrocyte decreased amount, abnormal
Acknowledgments:
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