{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T12:47:08Z","timestamp":1791290828238,"version":"4.3.0"},"reference-count":42,"publisher":"National Academy of Sciences","issue":"8","license":[{"start":{"date-parts":[[2009,8,24]],"date-time":"2009-08-24T00:00:00Z","timestamp":1251072000000},"content-version":"vor","delay-in-days":181,"URL":"http:\/\/www.pnas.org\/site\/misc\/userlicense.xhtml"}],"content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2009,2,24]]},"abstract":"<jats:p>\n                    The classical recessive coat color mutation\n                    <jats:italic>misty<\/jats:italic>\n                    (\n                    <jats:italic>m<\/jats:italic>\n                    ) arose spontaneously on the DBA\/J background and causes generalized hypopigmentation and localized white-spotting in mice, with a lack of pigment on the belly, tail tip, and paws. Here we describe\n                    <jats:italic>moonlight<\/jats:italic>\n                    (\n                    <jats:italic>mnlt<\/jats:italic>\n                    ), a second hypopigmentation and white-spotting mutation identified on the C57BL\/6J background, which yields a phenotypic copy of\n                    <jats:italic>m<\/jats:italic>\n                    \/\n                    <jats:italic>m<\/jats:italic>\n                    coat color traits. We demonstrate that the 2 mutations are allelic.\n                    <jats:italic>m<\/jats:italic>\n                    \/\n                    <jats:italic>m<\/jats:italic>\n                    and\n                    <jats:italic>mnlt<\/jats:italic>\n                    \/\n                    <jats:italic>mnlt<\/jats:italic>\n                    phenotypes both result from mutations that truncate the dedicator of cytokinesis 7 protein (DOCK7), a widely expressed Rho family guanine nucleotide exchange factor. Although\n                    <jats:italic>Dock7<\/jats:italic>\n                    is transcribed at high levels in the developing brain and has been implicated in both axon development and myelination by in vitro studies, we find no requirement for DOCK7 in neurobehavioral function in vivo. However, DOCK7 has non-redundant role(s) related to the distribution and function of dermal and follicular melanocytes.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0813208106","type":"journal-article","created":{"date-parts":[[2009,2,7]],"date-time":"2009-02-07T04:03:42Z","timestamp":1233979422000},"page":"2706-2711","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":39,"title":["Mice with mutations of\n                    <i>Dock7<\/i>\n                    have generalized hypopigmentation and white-spotting but show normal neurological function"],"prefix":"10.1073","volume":"106","author":[{"given":"Amanda L.","family":"Blasius","sequence":"first","affiliation":[{"name":"Departments of aGenetics and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katharina","family":"Brandl","sequence":"additional","affiliation":[{"name":"Departments of aGenetics 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