Fig. 1: Decreased AT2 cell numbers and differentiation after deletion of Prdm3/16. | Nature Communications

Fig. 1: Decreased AT2 cell numbers and differentiation after deletion of Prdm3/16.

From: PRDM3/16 regulate chromatin accessibility required for NKX2-1 mediated alveolar epithelial differentiation and function

Fig. 1

Immunofluorescence staining of embryonic lung indicates normal expression of NKX2-1 after deletion (a, e), loss of PRDM16 staining in lung epithelium in Prdm3/16ShhCreΔ/Δ fetuses and retention in vascular smooth muscle (b, f), n = 4 biological replicates. c, g Normal proximal (SOX2 + ) and distal (SOX9 + ) epithelial patterning is observed, n = 2 control and 4 mutant embryos. d, h At E14.5, the AT1 cell marker RAGE is increased in regions of Prdm3/16ShhCreΔ/Δ lungs, n = 3 biological replicates. i, m Hematoxylin and eosin staining of E18.5 lungs demonstrating poor sacculation in Prdm3/16ShhCreΔ/Δ n = 6 biological replicates. j, k, n, o Immunofluorescence staining for SFTPC and LAMP3 identifies AT2 cells; AT1 cells are stained for HOPX demonstrating paucity of AT2 cells and reduced LAMP3 expression, n = 3 biological replicates. l, p Electron microscopy of E18.5 lung demonstrates absence of mature lamellar bodies in the Prdm3/16ShhCreΔ/Δ AT2 cells, LB (lamellar body), M (mitochondria), n = 3 biological replicates. q Quantification of AT2, AT1, and AT2/AT1 cell numbers at E18.5 from 3 control and 3 Prdm3/16ShhCreΔ/Δ fetuses. p-values were calculated using a 2-tailed Mann-Whitney test.

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