Lung mesenchymal expression of Sox9 plays a critical role in tracheal development
1 Developmental Biology and Regenerative Medicine Program, Saban Research Institute, Children’s Hospital Los Angeles, Keck School of Medicine and Ostrow School of Dentistry, University of Southern California, 4661 Sunset Boulevard, Los Angeles, CA 90027, USA
2 Department of Genetics, University of Georgia, 120 East Green Street, Athens, GA 30602, USA
3 Department of Biosciences, Occidental College, 1600 Campus Road, Los Angeles, CA 90041, USA
BMC Biology 2013, 11:117 doi:10.1186/1741-7007-11-117Published: 25 November 2013
Additional file 1: Figure S1:
Lung phenotype after Sox9 knockout at embryonic day (E) 15.5. (A-D) Bright-field and dark-field pictures of (A, C) wild-type and (B, D) mutant Sox9 knockout mouse lungs. (E, F) Alcian blue staining of longitudinal sections of (E) wild-type and (F) mutant Sox9 knockout mouse trachea. C′ and D′ are high magnification pictures of C and D, respectively.
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Additional file 2: Figure S2:
Incomplete phenotype in Sox9Δ/Δ trachea. (A, B) A small percentage of the Sox9Δ/Δ lung developed proximal rudiments of cartilage in the ventral side of trachea. (C) Transverse section of lung in (B) stained for Sox9.
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Additional file 3: Figure S3:
Staining for P63 was used to determine changes in basal cells in E15.5 Sox9Δ/Δ trachea compared with Sox9fl/fl trachea. (A-C) Number of P63-positive cells in the tracheal epithelium was not affected by Sox9 deletion at embryonic day (E) 15.5.
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Additional file 4: Figure S4:
Sox2 and Foxp1 expression was not altered in Sox9Δ/Δ tracheal epithelium. Immunofluorescence staining for Sox2 and Foxp1 did not show any qualitative or quantitative alterations of expression of these transcriptional factors in the mutant trachea.
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