(
A) qPCR analysis on wildtype (Ctrl Kidney),
Rspo1-/- (R1 Ko),
CAGG:CreERTM; Rspo3fl/fl (R3 Ko) and on
CAGG:CreERTM, Rspo1-/-,
Rspo3fl/fl (R1 R3 Dbl Ko). For the conditional
Rspo3 allele, Tam induction was performed at E11.5 and kidneys were collected at E14.5. Data are expressed as fold change to highly expressing tissues (lung for
Rspo2, kidney for
Rspo3 and nail for
Rspo4). In wildtype kidneys, strong
Rspo3 expression was detected. By contrast,
Rspo2 and
Rspo4 showed little or no amplification, respectively. Tamoxifen-induced activation efficiently deleted
Rspo3. No compensatory upregulation of family members was observed. A one-way ANOVA test was performed. Analysis was performed on kidney pairs isolated from three mouse embryos (n = 3) for all samples except for (R1 R3 Dbl Ko) n = 2. See
Figure 1—figure supplement 1—source data 1. (
B)
Rspo3 is expressed in a subset of SIX2
+ nephron progenitors. In situ hybridisation (ISH) analysis carried out on wildtype embryonic kidneys followed by immunofluorescent analysis. (
C) In situ hybridisation (ISH) on E14.5 kidney sections prepared from control (Ctrl) and
Six2:Cre, Rspo3fl/fl animals. Immunofluorescence (IF) staining with anti-SIX2 antibodies was achieved on same sections to identify renal progenitors (red). ISH and IF signals were overlaid (green and red, respectively). Expression patterns within the nephrogenic niche are schematized to the right of the panel. Note the persistence of
Rspo3 expression in stromal cells upon progenitor-specific deletion (
Six2-Cre, Rspo3fl/fl animals).