TY - JOUR
T1 - Regulation of the human HBA genes by KLF4 in erythroid cell lines
AU - Marini, M. Giuseppina
AU - Porcu, Loredana
AU - Asunis, Isadora
AU - Loi, M. Giuseppina
AU - Ristaldi, M. Serafina
AU - Porcu, Susanna
AU - Ikuta, Tohru
AU - Cao, Antonio
AU - Moi, Paolo
PY - 2010/6
Y1 - 2010/6
N2 - KLF1/EKLF and related Krueppel-like factors (KLFs) are variably implicated in the regulation of the HBB-like globin genes. Prompted by the observation that four KLF sites are distributed in the human α-globin gene (HBA) promoter, we investigated if KLFs could also act to modulate the expression of the HBA genes. Among the KLFs tested, only KLF4/GKLF bound specifically to three out of four α-globin KLF sites. The occupancy of the same sites by KLF4 in vivo was confirmed by chromatin immunoprecipitation assays with KLF4-specific antibodies. In luciferase reporter assays in MEL cells, high levels of the wild type HBA promoter, but not mutated promoters bearing point mutations that disrupted KLF4-DNA binding, were transactivated by over-expression of KLF4. In K562 cells, induced KLF4 expression with a Tet-off regulated cassette stimulated the expression of the endogenous HBA genes. In a complementary assay in the same cell line, knocking down KLF4 with lentiviral delivered sh-RNAs caused a parallel decrease in the transcription of the HBA genes. All experiments combined support a regulatory role of KLF4 in the control of HBA gene expression.
AB - KLF1/EKLF and related Krueppel-like factors (KLFs) are variably implicated in the regulation of the HBB-like globin genes. Prompted by the observation that four KLF sites are distributed in the human α-globin gene (HBA) promoter, we investigated if KLFs could also act to modulate the expression of the HBA genes. Among the KLFs tested, only KLF4/GKLF bound specifically to three out of four α-globin KLF sites. The occupancy of the same sites by KLF4 in vivo was confirmed by chromatin immunoprecipitation assays with KLF4-specific antibodies. In luciferase reporter assays in MEL cells, high levels of the wild type HBA promoter, but not mutated promoters bearing point mutations that disrupted KLF4-DNA binding, were transactivated by over-expression of KLF4. In K562 cells, induced KLF4 expression with a Tet-off regulated cassette stimulated the expression of the endogenous HBA genes. In a complementary assay in the same cell line, knocking down KLF4 with lentiviral delivered sh-RNAs caused a parallel decrease in the transcription of the HBA genes. All experiments combined support a regulatory role of KLF4 in the control of HBA gene expression.
KW - Erythroid regulation
KW - GKLF
KW - HBA gene expression
KW - KLF4
KW - Krueppel-like factors
KW - ShRNA
KW - α-globin gene
UR - http://www.scopus.com/inward/record.url?scp=77952662441&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77952662441&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2141.2010.08130.x
DO - 10.1111/j.1365-2141.2010.08130.x
M3 - Article
C2 - 20331458
AN - SCOPUS:77952662441
SN - 0007-1048
VL - 149
SP - 748
EP - 758
JO - British Journal of Haematology
JF - British Journal of Haematology
IS - 5
ER -