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Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.

Hereditary persistence of fetal hemoglobin (HPFH) can involve large deletions which eliminate the 3' end of the beta-like globin gene cluster and more than 70 kilobases (kb) of flanking DNA. Blot hybridization revealed a DNase I-hypersensitive site extending from 1.1 to 1.4 kb downstream of the...

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Prif Awduron:	Elder, J T, Forrester, W C, Thompson, C, Mager, D, Henthorn, P, Peretz, M, Papayannopoulou, T, Groudine, M
Fformat:	Erthygl
Iaith:	en
Cyhoeddwyd:	1990
Pynciau:	Research Article
Mynediad Ar-lein:	https://ncbi.nlm.nih.gov/pmc/articles/PMC362240/ https://ncbi.nlm.nih.gov/pubmed/1690839
Tagiau:	Ychwanegu Tag Dim Tagiau, Byddwch y cyntaf i dagio'r cofnod hwn!

id	pubmed-362240
record_format	dspace
spelling	pubmed-3622402004-03-11 Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin. Elder, J T Forrester, W C Thompson, C Mager, D Henthorn, P Peretz, M Papayannopoulou, T Groudine, M Mol Cell Biol Research Article Hereditary persistence of fetal hemoglobin (HPFH) can involve large deletions which eliminate the 3' end of the beta-like globin gene cluster and more than 70 kilobases (kb) of flanking DNA. Blot hybridization revealed a DNase I-hypersensitive site extending from 1.1 to 1.4 kb downstream of the HPFH-1 3' deletion endpoint. The site was found in normal fetal and adult nucleated erythroid cells and in two erythroleukemia cell lines but not in nonerythroid cells and tissues. Simian virus 40 core enhancer-like sequences were found nonrandomly distributed within the boundaries of the site, which is contained in a fragment of known enhancer activity (E. A. Feingold and B. G. Forget, Blood, in press). A second hypersensitive site was found 0.5 kb upstream of the HPFH-1 3' deletion endpoint but was not erythroid specific. A third site, most prominent in fetal liver-derived erythroid cells, was found 1 kb upstream of the HPFH-2 deletion endpoint. As predicted by the locations of the deletion endpoints, the first two sites were translocated to within 12 kb of the A gamma gene in erythroid colonies derived from an HPFH-2 heterozygote and in hybrid mouse-human erythroid cells carrying the HPFH-2 deletion chromosome. Further analysis of this region showed that it was DNase I sensitive in erythroid and myeloid cells, indicating that it resides in an open chromatin domain. These observations suggest that alterations of chromatin structure flanking the fetal globin genes may contribute to abnormal gene regulation in deletion-type HPFH. 1990-04 /pmc/articles/PMC362240/ /pubmed/1690839 Text en
institution	US National Library of Medicine
collection	PubMed Central
language	en
format	Article
topic	Research Article
spellingShingle	Research Article Elder, J T Forrester, W C Thompson, C Mager, D Henthorn, P Peretz, M Papayannopoulou, T Groudine, M Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
description	Hereditary persistence of fetal hemoglobin (HPFH) can involve large deletions which eliminate the 3' end of the beta-like globin gene cluster and more than 70 kilobases (kb) of flanking DNA. Blot hybridization revealed a DNase I-hypersensitive site extending from 1.1 to 1.4 kb downstream of the HPFH-1 3' deletion endpoint. The site was found in normal fetal and adult nucleated erythroid cells and in two erythroleukemia cell lines but not in nonerythroid cells and tissues. Simian virus 40 core enhancer-like sequences were found nonrandomly distributed within the boundaries of the site, which is contained in a fragment of known enhancer activity (E. A. Feingold and B. G. Forget, Blood, in press). A second hypersensitive site was found 0.5 kb upstream of the HPFH-1 3' deletion endpoint but was not erythroid specific. A third site, most prominent in fetal liver-derived erythroid cells, was found 1 kb upstream of the HPFH-2 deletion endpoint. As predicted by the locations of the deletion endpoints, the first two sites were translocated to within 12 kb of the A gamma gene in erythroid colonies derived from an HPFH-2 heterozygote and in hybrid mouse-human erythroid cells carrying the HPFH-2 deletion chromosome. Further analysis of this region showed that it was DNase I sensitive in erythroid and myeloid cells, indicating that it resides in an open chromatin domain. These observations suggest that alterations of chromatin structure flanking the fetal globin genes may contribute to abnormal gene regulation in deletion-type HPFH.
author	Elder, J T Forrester, W C Thompson, C Mager, D Henthorn, P Peretz, M Papayannopoulou, T Groudine, M
author_facet	Elder, J T Forrester, W C Thompson, C Mager, D Henthorn, P Peretz, M Papayannopoulou, T Groudine, M
author_sort	Elder, J T
title	Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
title_short	Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
title_full	Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
title_fullStr	Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
title_full_unstemmed	Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
title_sort	translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.
publishDate	1990
url	https://ncbi.nlm.nih.gov/pmc/articles/PMC362240/ https://ncbi.nlm.nih.gov/pubmed/1690839
_version_	1759383396465770496

Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.

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