{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T03:34:22Z","timestamp":1790739262745,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,2,12]],"date-time":"2020-02-12T00:00:00Z","timestamp":1581465600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["anatomypubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Hemicentins (HMCNs) are a family of extracellular matrix proteins first identified in <jats:styled-content style=\"fixed-case\"><jats:italic>Caenorhabditis elegans<\/jats:italic><\/jats:styled-content>, with two orthologs (HMCN1 and 2) in vertebrates. In worms, HMCN is deposited at specific sites where it forms long, fine tracks that link two tissues by connecting adjacent basement membranes (BMs). By generating CRISPR\/Cas9\u2010mediated <jats:italic>Hmcn1<\/jats:italic> and <jats:italic>Hmcn2<\/jats:italic> knockout mice, we tested the hypothesis that HMCNs perform similar functions in mammals.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Hmcn1<\/jats:italic><jats:sup>\n<jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice were viable and fertile. Using new, knockout mouse\u2010validated HMCN1 antibodies, HMCN1 was detected in wild\u2010type mice as fine tracks along the BM of hair and whisker follicles, in the sclera of the eyes, and in the lumen of some lymphoid conduits. It was also observed in the mesangial matrix of the kidney glomerulus. However, HMCN1 deficiency did not affect the functions of these tissues, including adherence of coat hairs and whiskers, the sieving function of lymphoid conduits, or the immune response to injected antigens. HMCN2 deficiency did not lead to any discernible phenotypes on its own or when combined with HMCN1 deficiency.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>That <jats:italic>Hmcn1<\/jats:italic><jats:sup>\n<jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>, <jats:italic>Hmcn2<\/jats:italic><jats:sup>\n<jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>, and <jats:italic>Hmcn1\/2<\/jats:italic> double knockout mice did not display any overt phenotypes implicates compensation by other members of the fibulin family.<\/jats:p><\/jats:sec>","DOI":"10.1002\/dvdy.159","type":"journal-article","created":{"date-parts":[[2020,2,8]],"date-time":"2020-02-08T12:25:09Z","timestamp":1581164709000},"page":"775-788","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Mammalian hemicentin 1 is assembled into tracks in the extracellular matrix of multiple 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