Research Article

Secretoglobin Superfamily Protein SCGB3A2 Deficiency Potentiates Ovalbumin-Induced Allergic Pulmonary Inflammation

Figure 1

Generation of Scgb3a2 knockout mice. (a) Schematic of wild-type (top), floxed-Neo (middle), and knockout (bottom) alleles after Cre-mediated excision of exons 2 and 3. Scgb3a2 exons 1, 2, and 3 are indicated by boxes. (b) DNA from wild-type ES cells (+/+) and floxed cell clone (+/fl) were digested with Pst I and subjected to Southern blot hybridization using the downstream of the 3rd exon as a 3′ probe (left panel). Tail DNA from F1 progeny of two single floxed-Scgb3a2 (+/fl) intercrosses was digested with Spe I and subjected to Southern blot hybridization using the sequence upstream of the 1st exon as a 5′ probe (right panel). The genotype for the Scgb3a2 locus was indicated above each lane. Sizes of the DNA fragments were indicated on the right in the parenthesis. Restriction sites and location of the 3′ and 5′ probes are indicated in (a). (c) Double floxed-Scgb3a2 (fl/fl) mice were crossed with EIIA-Cre transgenic mice expressing Cre in germ cells. Tail genome from F1 progeny of two heterozygote intercrosses was genotyped by PCR using wild-type (WT) primers and knockout (KO) primers to amplify either the WT (227 bp long, left panel) or the KO allele (362 bp long, right panel). The genotype for the Scgb3a2 locus was indicated above each lane. Primer positions are indicated in (a).
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(a)
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(b)
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(c)