Fig. 4

PCDH20 deficiency impaired epithelial barrier integrity in colitis by disrupted adherens junctions. a,b Gene ontology (GO) terms of the top regulated cellular components in phosphoproteomics of colon of Pcdh20 CKO mice with DSS-induced colitis (n = 3). Bubble graph of top 20 cellular components (a), adherens junctions ranked first in top 8 cellular components (b). c–e Distinct gap in adherens junction (c, red arrows in d), but not tight junction (yellow arrows in d) and shorten microvilli (e, red arrows) in the colon epithelium of Pcdh20 CKO mice at day 10 after DSS administration, observed by transmission electron microscope. Magnification: × 3000 (c), × 10,000 (zooming box, c), × 40,000 (d), × 8000 (e); scale bars = 1 μm (c, e) and 200 nm (zooming box in c, d). Representative images, n = 3. f Phosphoproteomics analysis on the phosphorylation sites of adherens junctions proteins in Pcdh20 CKO mice with DSS-induced colitis (n = 3). g,h Immunoblots of adherens junctions components in Pcdh20 CKO mice with DSS-induced colitis (g) and cell lines with stable PCDH20 knockdown and overexpression under the treatment of TNFα (2.5 ng/mL) and IFN-γ (10 ng/mL) (h)