Search for basonuclin target genes

Wang, Junwen; Zhang, Shengliang; Schultz, Richard M.; Tseng, Hung

doi:10.1016/j.bbrc.2006.07.198

Cited by 29 publications

(36 citation statements)

References 41 publications

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“…12 The predicted BNC2 protein is about 1100 amino acids in length and contains a nuclear localization signal and three zinc-finger motifs, 13,14 with a similar overall structure to Basonuclin 1 (BNC1), a protein found in keratinocytes 15 and germ cells 16 that acts as a transcription factor for ribosomal RNA 17,18 and possibly also RNA polymerase II-dependent genes. 19 BNC1 and BNC2 show nonoverlapping patterns of expression, and BNC2 but not BNC1 localizes to nuclear speckles, suggesting that BNC2 functions in mRNA processing. 20 Bnc2 À/À knockout mice die perinatally, with cleft palate and other craniofacial abnormalities.…”

Section: Introductionmentioning

confidence: 97%

Human balanced translocation and mouse gene inactivation implicate Basonuclin 2 in distal urethral development

et al. 2011

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We studied a man with distal hypospadias, partial anomalous pulmonary venous return, mild limb-length inequality and a balanced translocation involving chromosomes 9 and 13. To gain insight into the etiology of his birth defects, we mapped the translocation breakpoints by high-resolution comparative genomic hybridization (CGH), using chromosome 9-and 13-specific tiling arrays to analyze genetic material from a spontaneously aborted fetus with unbalanced segregation of the translocation. The chromosome 13 breakpoint was B400 kb away from the nearest gene, but the chromosome 9 breakpoint fell within an intron of Basonuclin 2 (BNC2), a gene that encodes an evolutionarily conserved nuclear zinc-finger protein. The BNC2/Bnc2 gene is abundantly expressed in developing mouse and human periurethral tissues. In all, 6 of 48 unrelated subjects with distal hypospadias had nine novel nonsynonymous substitutions in BNC2, five of which were computationally predicted to be deleterious. In comparison, two of 23 controls with normal penile urethra morphology, each had a novel nonsynonymous substitution in BNC2, one of which was predicted to be deleterious. Bnc2 À/À mice of both sexes displayed a high frequency of distal urethral defects; heterozygotes showed similar defects with reduced penetrance. The association of BNC2 disruption with distal urethral defects and the gene's expression pattern indicate that it functions in urethral development.

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Section: Introductionmentioning

confidence: 97%

Human balanced translocation and mouse gene inactivation implicate Basonuclin 2 in distal urethral development

et al. 2011

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“…The alpha-hB34 antibody precipitated from HaCaT cell extract a protein with molecular weight identical to that of basonuclin (i.e., 120k)( Fig. 1A ) [3], [9], [10]. The amount of antibody used was sufficient to remove all soluble basonuclin ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Basonuclin Regulates a Subset of Ribosomal RNA Genes in HaCaT Cells

2007

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Basonuclin (Bnc1), a cell-type-specific ribosomal RNA (rRNA) gene regulator, is expressed mainly in keratinocytes of stratified epithelium and gametogenic cells of testis and ovary. Previously, basonuclin was shown in vitro to interact with rRNA gene (rDNA) promoter at three highly conserved sites. Basonuclin's high affinity binding site overlaps with the binding site of a dedicated and ubiquitous Pol I transcription regulator, UBF, suggesting that their binding might interfere with each other if they bind to the same promoter. Knocking-down basonuclin in mouse oocytes eliminated approximately one quarter of RNA polymerase I (Pol I) transcription foci, without affecting the BrU incorporation of the remaining ones, suggesting that basonuclin might regulate a subset of rDNA. Here we show, via chromatin immunoprecipitation (ChIP), that basonuclin is associated with rDNA promoters in HaCaT cells, a spontaneously established human keratinocyte line. Immunoprecipitation data suggest that basonuclin is in a complex that also contains the subunits of Pol I (RPA194, RPA116), but not UBF. Knocking-down basonuclin in HaCaT cells partially impairs the association of RPA194 to rDNA promoter, but not that of UBF. Basonuclin-deficiency also reduces the amount of 47S pre-rRNA, but this effect can be seen only after cell-proliferation related rRNA synthesis has subsided at a higher cell density. DNA sequence of basonuclin-bound rDNA promoters shows single nucleotide polymorphisms (SNPs) that differ from those associated with UBF-bound promoters, suggesting that basonuclin and UBF interact with different subsets of promoters. In conclusion, our results demonstrate basonuclin's functional association with rDNA promoters and its interaction with Pol I in vivo. Our data also suggest that basonuclin-Pol I complex transcribes a subset of rDNA.

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“…We used known PU.1 binding sites from the TRANSFAC database (23) and constructed a propensity model (49) to capture the interdependency among the individual binding site positions. We then scanned the putative PU.1 binding sites in bp Ϫ500 to ϩ100 promoter regions around each transcription start site in human and mouse (50). We used a sliding window of size 8 (the length of PU.1 binding site) to scan along the 600-bp promoter sequence and recorded the P value for each window by the computational model.…”

Section: Dna Constructsmentioning

confidence: 99%

PU.1 Can Recruit BCL6 to DNA To Repress Gene Expression in Germinal Center B Cells

Wei

Zaprazna

Wang

et al. 2009

Molecular and Cellular Biology

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BCL6 is a transcriptional repressor crucial for germinal center formation. BCL6 represses transcription by a variety of mechanisms by binding to specific DNA sequences or by recruitment to DNA by protein interactions. We found that BCL6 can inhibit activities of the immunoglobulin kappa (Ig) intron and 3 enhancers. At the Ig 3 enhancer, BCL6 repressed enhancer activity through the PU.1 binding site. We found that BCL6 physically interacted with PU.1 in vivo and in vitro, and the results of sequential chromatin immunoprecipitation assays and transient-expression assays suggested that BCL6 recruitment to the Ig and Ig 3 enhancers occurred via PU.1 interaction. By computational studies, we identified genes that are repressed in germinal center cells and whose promoters contain conserved PU.1 binding sites in mouse and human. We found that many of these promoters bound to both PU.1 and BCL6 in vivo. In addition, BCL6 knockdown resulted in increased expression of a subset of these genes, demonstrating that BCL6 is involved in their repression. The recruitment of BCL6 to promoter regions by PU.1 represents a new regulatory mechanism that expands the number of genes regulated by this important transcriptional repressor.The B-cell lymphoma 6 (BCL6) gene was identified on the basis of its location at chromosomal breakpoints in nonHodgkin's disease B-cell lymphomas (7, 55). About 30% of diffuse large cell lymphoma cases contain translocations between the BCL6 locus at chromosome 3q27 and other genes (7,11,55). BCL6 belongs to the BTB-POZ zinc finger family of transcription factors and contains Kruppel-type zinc finger motifs at the carboxyl terminus and a POZ motif at the amino terminus. The six BCL6 zinc fingers bind to the consensus DNA sequence TTCCT(A/C)GAA (9, 39), and the BCL6 POZ domain physically interacts with corepressor proteins, including nuclear receptor corepressor (N-CoR), BCL-6-interacting corepressor (B-CoR), SMRT (silencing mediator of retinoid acid and thyroid hormone receptor)/mSIN3A (mammalian SIN3A), Mi-2/NURD (nucleosome remodeling and histone deacetylation), and histone deacetylase complexes to mediate its potent transrepressor activity (1,12,13,18,21,52,57).BCL6 plays crucial roles in germinal center biology. Knockout studies revealed that bcl6 Ϫ/Ϫ mice fail to develop germinal centers, lack affinity maturation, and mount reduced levels of antigen-specific antibody responses (10,14,54). In addition, inhibition of BCL6 function in B-cell lines initiates changes characteristic of plasma cell differentiation (40). BCL6 is thought to exert its effect on germinal center development by modulating the transcription of genes involved in cell cycle regulation, proliferation, activation, class switch recombination, and differentiation. BCL6 can repress a variety of genes, including Blimp-1, ATR (ataxia-telangiectasia and Rad3-related), CD80, p53, programmed cell death2, monocyte chemotactic peptide 1 (MCP-1), MCP-3, multidrug resistance-associated protein 1 (MRP1), and interleukin 18 (6,22,27,30,36,37,40,43...

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Search for basonuclin target genes

Cited by 29 publications

References 41 publications

Human balanced translocation and mouse gene inactivation implicate Basonuclin 2 in distal urethral development

Human balanced translocation and mouse gene inactivation implicate Basonuclin 2 in distal urethral development

Basonuclin Regulates a Subset of Ribosomal RNA Genes in HaCaT Cells

PU.1 Can Recruit BCL6 to DNA To Repress Gene Expression in Germinal Center B Cells

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