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  • 1
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    Developmental and species-divergent globin switching are driven by BCL11A (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-08-07
    Description: The contribution of changes in cis-regulatory elements or trans-acting factors to interspecies differences in gene expression is not well understood. The mammalian beta-globin loci have served as a model for gene regulation during development. Transgenic mice containing the human beta-globin locus, consisting of the linked embryonic (epsilon), fetal (gamma) and adult (beta) genes, have been used as a system to investigate the temporal switch from fetal to adult haemoglobin, as occurs in humans. Here we show that the human gamma-globin (HBG) genes in these mice behave as murine embryonic globin genes, revealing a limitation of the model and demonstrating that critical differences in the trans-acting milieu have arisen during mammalian evolution. We show that the expression of BCL11A, a repressor of human gamma-globin expression identified by genome-wide association studies, differs between mouse and human. Developmental silencing of the mouse embryonic globin and human gamma-globin genes fails to occur in mice in the absence of BCL11A. Thus, BCL11A is a critical mediator of species-divergent globin switching. By comparing the ontogeny of beta-globin gene regulation in mice and humans, we have shown that alterations in the expression of a trans-acting factor constitute a critical driver of gene expression changes during evolution.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749913/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3749913/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sankaran, Vijay G -- Xu, Jian -- Ragoczy, Tobias -- Ippolito, Gregory C -- Walkley, Carl R -- Maika, Shanna D -- Fujiwara, Yuko -- Ito, Masafumi -- Groudine, Mark -- Bender, M A -- Tucker, Philip W -- Orkin, Stuart H -- P01 HL032262/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Aug 27;460(7259):1093-7. doi: 10.1038/nature08243. Epub 2009 Aug 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital Boston and Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Stem Cell Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19657335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Embryo, Mammalian/metabolism ; Evolution, Molecular ; Fetus/metabolism ; *Gene Expression Regulation, Developmental ; Gene Silencing ; Globins/*genetics ; Hematopoiesis ; Humans ; Mice ; Nuclear Proteins/genetics/*metabolism ; Species Specificity ; beta-Globins/genetics ; gamma-Globins/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Natural malaria infection in Anopheles gambiae is regulated by a single genomic control region (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: We surveyed an Anopheles gambiae population in a West African malaria transmission zone for naturally occurring genetic loci that control mosquito infection with the human malaria parasite, Plasmodium falciparum. The strongest Plasmodium resistance loci cluster in a small region of chromosome 2L and each locus explains at least 89% of parasite-free mosquitoes in independent pedigrees. Together, the clustered loci form a genomic Plasmodium-resistance island that explains most of the genetic variation for malaria parasite infection of mosquitoes in nature. Among the candidate genes in this chromosome region, RNA interference knockdown assays confirm a role in Plasmodium resistance for Anopheles Plasmodium-responsive leucine-rich repeat 1 (APL1), encoding a leucine-rich repeat protein that is similar to molecules involved in natural pathogen resistance mechanisms in plants and mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riehle, Michelle M -- Markianos, Kyriacos -- Niare, Oumou -- Xu, Jiannong -- Li, Jun -- Toure, Abdoulaye M -- Podiougou, Belco -- Oduol, Frederick -- Diawara, Sory -- Diallo, Mouctar -- Coulibaly, Boubacar -- Ouatara, Ahmed -- Kruglyak, Leonid -- Traore, Sekou F -- Vernick, Kenneth D -- New York, N.Y. -- Science. 2006 Apr 28;312(5773):577-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Microbial and Plant Genomics and Department of Microbiology, University of Minnesota, St. Paul, MN 55108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645095" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anopheles gambiae/*genetics/immunology/*parasitology ; Chromosome Mapping ; Female ; *Genes, Insect ; Genetic Linkage ; Genetic Variation ; Genome, Insect ; Humans ; Immunity, Innate/genetics ; Insect Proteins/*genetics/physiology ; Insect Vectors/genetics/*parasitology ; Malaria, Falciparum/parasitology ; Male ; Mali ; Oligonucleotide Array Sequence Analysis ; Pedigree ; Phenotype ; Plasmodium berghei/immunology/pathogenicity ; Plasmodium falciparum/immunology/*pathogenicity ; RNA Interference
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: Differences in the amount of fetal hemoglobin (HbF) that persists into adulthood affect the severity of sickle cell disease and the beta-thalassemia syndromes. Genetic association studies have identified sequence variants in the gene BCL11A that influence HbF levels. Here, we examine BCL11A as a potential regulator of HbF expression. The high-HbF BCL11A genotype is associated with reduced BCL11A expression. Moreover, abundant expression of full-length forms of BCL11A is developmentally restricted to adult erythroid cells. Down-regulation of BCL11A expression in primary adult erythroid cells leads to robust HbF expression. Consistent with a direct role of BCL11A in globin gene regulation, we find that BCL11A occupies several discrete sites in the beta-globin gene cluster. BCL11A emerges as a therapeutic target for reactivation of HbF in beta-hemoglobin disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sankaran, Vijay G -- Menne, Tobias F -- Xu, Jian -- Akie, Thomas E -- Lettre, Guillaume -- Van Handel, Ben -- Mikkola, Hanna K A -- Hirschhorn, Joel N -- Cantor, Alan B -- Orkin, Stuart H -- HL32259-27/HL/NHLBI NIH HHS/ -- HL32262-26/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Dec 19;322(5909):1839-42. doi: 10.1126/science.1165409. Epub 2008 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Children's Hospital Boston, Harvard Stem Cell Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics/metabolism ; Cell Line, Tumor ; Cells, Cultured ; Down-Regulation ; Erythroblasts/metabolism ; Erythroid Cells/*metabolism ; Erythroid Precursor Cells/metabolism ; Erythropoiesis ; Fetal Hemoglobin/biosynthesis/*genetics ; GATA1 Transcription Factor/metabolism ; *Gene Expression Regulation ; Hemoglobinopathies/therapy ; Histone Deacetylases/metabolism ; Humans ; K562 Cells ; Mi-2 Nucleosome Remodeling and Deacetylase Complex ; Mice ; Multigene Family ; Nuclear Proteins/*genetics/metabolism ; Polymorphism, Single Nucleotide ; Protein Isoforms/genetics/metabolism ; RNA Interference ; Transcription Factors/metabolism ; Transcription, Genetic ; beta-Globins/genetics/metabolism ; gamma-Globins/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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