{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T14:51:28Z","timestamp":1781103088580,"version":"3.54.1"},"reference-count":0,"publisher":"National Academy of Sciences","issue":"14","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1992,7,15]]},"abstract":"<jats:p>Several overlapping chromosomal deletions spanning the albino locus in the mouse cause perinatal lethality when homozygous and a block in the transcriptional induction of various unlinked hepatocyte-specific genes. Studies of such lethal albino deletion homozygotes in perinatal stages revealed a deficiency in the transcriptional inducibility of the tyrosine aminotransferase (TAT) gene by glucocorticoids; yet, glucocorticoid receptor and hormone levels were shown to be unaffected. To identify a molecular defect underlying the failure of inducible expression, we examined the chromatin structure of the TAT gene. Whereas in wild-type animals the TAT promoter becomes DNase I hypersensitive at birth, such hypersensitivity fails to develop in lethal albino deletion homozygotes. By contrast, the deletions do not affect the appearance of three DNase I-hypersensitive sites upstream of the TAT promoter in the liver, nor do they affect two hypersensitive sites upstream of the expressed alpha-fetoprotein gene. These findings demonstrate that the abnormality of chromatin structure identified in lethal albino deletion homozygotes occurs on a highly selective basis. Specifically, normal differentiation of the TAT promoter chromatin appears to depend directly or indirectly on the action and product of a gene mapping within the deleted region.<\/jats:p>","DOI":"10.1073\/pnas.89.14.6540","type":"journal-article","created":{"date-parts":[[2006,5,31]],"date-time":"2006-05-31T08:05:05Z","timestamp":1149062705000},"page":"6540-6544","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":7,"title":["Selective loss of a DNase I hypersensitive site upstream of the tyrosine aminotransferase gene in mice homozygous for lethal albino deletions."],"prefix":"10.1073","volume":"89","author":[{"given":"K S","family":"Zaret","sequence":"first","affiliation":[{"name":"Section of Biochemistry, Brown University, Providence, RI 02912."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Milos","sequence":"additional","affiliation":[{"name":"Section of Biochemistry, Brown University, Providence, RI 02912."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Lia","sequence":"additional","affiliation":[{"name":"Section of Biochemistry, Brown University, Providence, RI 02912."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"Bali","sequence":"additional","affiliation":[{"name":"Section of Biochemistry, Brown University, Providence, RI 02912."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Gluecksohn-Waelsch","sequence":"additional","affiliation":[{"name":"Section of Biochemistry, Brown University, Providence, RI 02912."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[1992,7,15]]},"container-title":["Proceedings of the National Academy of Sciences"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/pnas.org\/doi\/pdf\/10.1073\/pnas.89.14.6540","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,4,13]],"date-time":"2022-04-13T13:01:35Z","timestamp":1649854895000},"score":1,"resource":{"primary":{"URL":"https:\/\/pnas.org\/doi\/full\/10.1073\/pnas.89.14.6540"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1992,7,15]]},"references-count":0,"journal-issue":{"issue":"14","published-print":{"date-parts":[[1992,7,15]]}},"alternative-id":["10.1073\/pnas.89.14.6540"],"URL":"https:\/\/doi.org\/10.1073\/pnas.89.14.6540","relation":{},"ISSN":["0027-8424","1091-6490"],"issn-type":[{"value":"0027-8424","type":"print"},{"value":"1091-6490","type":"electronic"}],"subject":[],"published":{"date-parts":[[1992,7,15]]},"assertion":[{"value":"1992-07-15","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}