Fig. 6: Inducible losses of FPN1 and ZIP13 resulted in strong and distinctive iron dyshomeostasis patterns.
From: Mammalian SLC39A13 promotes ER/Golgi iron transport and iron homeostasis in multiple compartments

a Fpn1-iKO and Zip13-iKO mice displayed similar hunchback symptoms. b HE (left) and Masson (right, blue) staining of mouse skins. Scale bar, 200 μm. c Levels of collagen hydroxylation were measured by LC-MS. The ratios of collagen hydroxylation to nonhydroxylation relative to that of WT were shown. d Iron supplementation increased the collage thickness of the skin in Fpn1-iKO mice, but not in Zip13-iKO mice (blue). Scale bar, 200 μm. e Fpn1-iKO mice were pale and bloodless, but Zip13-iKO mice were not. f Levels of serum iron in WT, Fpn1-iKO, and Zip13-iKO mice (n = 8, biologically independent replicates). g Spleens of WT, Fpn1-iKO, and Zip13-iKO mice. h, Perls’ staining of some tissues in WT, Fpn1-iKO, and Zip13-iKO mice. Intestine, heart, liver, and kidney: brown; Spleen: blue. Scale bar, 200 μm. Each experiment was repeated independently at least three times with similar results (b–h). Data are mean ± SD. Statistical analysis was performed using two-tailed student’s t-test (f). Source data are provided as a Source Data file.