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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: Cell. 2010 Jul 15;142(2):203–217. doi: 10.1016/j.cell.2010.06.001

Figure 4. Characterization of homozygous Srd5a3Gt/Gt gene trap mouse embryos.

Figure 4

(A) Phenotype at E10.5 shows failure to rotate, ventral body wall defect (arrow) and dilated heart (arrowhead). Scale bar 1 mm.

(B) Graphic representation of the genotype obtained from the progeny of heterozygous mating, with lethality appearing between E11.5 and E13.5.

(C) Genes overexpressed in Srd5a3Gt/Gt at E8.5 detected using 44k mouse genome oligo microarray (1 is the Log 2 of a 2 fold expression increase, error bars represent the mean +/− standard deviation from 4 independent experiments). Among 10 of the most upregulated genes, 5 (in blue) are involved in the unfolded protein response pathway UPR). Morphology of heterozygous and homozygous Srd5a3 mutant embryos at E8.5, before embryo axial rotation. Scale bar 500 µm.

(D) Real-time RT-PCR confirming activation of the UPR pathway (Errors bars are means +/− standard deviations, asterisks indicate p<0.05, n=3).

(E) Immunofluorescence staining showing expression of BiP protein (red), a marker of the UPR pathway activation, in the neuroepithelium of the forebrain vesicle (arrowheads). Scale bar 50µm.

See also Figure S4.