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Effect of FoxA-deletion on <t>HBV</t> <t>DNA</t> methylation distribution in adult mouse liver. The CpG DNA methylation frequency distribution across the 11, 38 and 14 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2131–2441, respectively, from male (A, C and E) and female (B, D and F) FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-); M A1A2A3Cre(-) and F A1A2A3Cre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+); M A1A2A3Cre(+) and F A1A2A3Cre(+)) HBV transgenic mice is shown.
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Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

Journal: PLoS Pathogens

doi: 10.1371/journal.ppat.1006239

Effect of FoxA-deletion on HBV DNA methylation distribution in adult mouse liver. The CpG DNA methylation frequency distribution across the 11, 38 and 14 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2131–2441, respectively, from male (A, C and E) and female (B, D and F) FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-); M A1A2A3Cre(-) and F A1A2A3Cre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+); M A1A2A3Cre(+) and F A1A2A3Cre(+)) HBV transgenic mice is shown.
Figure Legend Snippet: Effect of FoxA-deletion on HBV DNA methylation distribution in adult mouse liver. The CpG DNA methylation frequency distribution across the 11, 38 and 14 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2131–2441, respectively, from male (A, C and E) and female (B, D and F) FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-); M A1A2A3Cre(-) and F A1A2A3Cre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+); M A1A2A3Cre(+) and F A1A2A3Cre(+)) HBV transgenic mice is shown.

Techniques Used: DNA Methylation Assay, Expressing, Transgenic Assay, Mouse Assay

RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of 1, 2, 3, 4 and 7 week old HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A1A2A3). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. The levels of the transcripts which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p
Figure Legend Snippet: RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of 1, 2, 3, 4 and 7 week old HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A1A2A3). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. The levels of the transcripts which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

Techniques Used: Northern Blot, Hybridization, Quantitative RT-PCR, Transgenic Assay, Mouse Assay, Expressing, Quantitation Assay

RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of adult HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. Average number of mice per group was 6.6±1.9 (Range: 4–9). The levels of the HBV 3.5kb transcript which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p
Figure Legend Snippet: RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of adult HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. Average number of mice per group was 6.6±1.9 (Range: 4–9). The levels of the HBV 3.5kb transcript which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

Techniques Used: Northern Blot, Hybridization, Quantitative RT-PCR, Transgenic Assay, Mouse Assay, Expressing, Quantitation Assay

Tissue-specific and developmental regulation of HBV DNA methylation. (A) The percentage of CpG DNA methylation at each position within the HBV genome from a male (A) and female (B) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The percentage of CpG DNA methylation at each position within the HBV genome from three individual 0.5 day old neonatal wild-type HBV transgenic mouse livers is shown.
Figure Legend Snippet: Tissue-specific and developmental regulation of HBV DNA methylation. (A) The percentage of CpG DNA methylation at each position within the HBV genome from a male (A) and female (B) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The percentage of CpG DNA methylation at each position within the HBV genome from three individual 0.5 day old neonatal wild-type HBV transgenic mouse livers is shown.

Techniques Used: DNA Methylation Assay, Transgenic Assay, Binding Assay

DNA (Southern) filter hybridization analysis of HBV DNA replication intermediates in the livers of adult HBV transgenic mice. (A) DNA (Southern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probe used was HBVayw genomic DNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The HBV transgene (Tg) was used as an internal control for the quantitation of the HBV replication intermediates. Tg = HBV transgene; RC = HBV relaxed circular replication intermediates; SS = HBV single stranded replication intermediates. (B) Quantitative analysis of the HBV DNA replication intermediate (RI) levels in HBV transgenic mice. The mean DNA replication intermediate levels plus standard deviations are indicated. Average number of mice per group was 6.7±1.8 (Range: 4–9). The levels of replication intermediates which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p
Figure Legend Snippet: DNA (Southern) filter hybridization analysis of HBV DNA replication intermediates in the livers of adult HBV transgenic mice. (A) DNA (Southern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probe used was HBVayw genomic DNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The HBV transgene (Tg) was used as an internal control for the quantitation of the HBV replication intermediates. Tg = HBV transgene; RC = HBV relaxed circular replication intermediates; SS = HBV single stranded replication intermediates. (B) Quantitative analysis of the HBV DNA replication intermediate (RI) levels in HBV transgenic mice. The mean DNA replication intermediate levels plus standard deviations are indicated. Average number of mice per group was 6.7±1.8 (Range: 4–9). The levels of replication intermediates which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

Techniques Used: Hybridization, Transgenic Assay, Mouse Assay, Expressing, Quantitation Assay

Tissue-specific and developmental regulation of HBV DNA methylation distribution. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from male (A-C) and female (D-F) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain DNA is shown. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from three independent 0.5 day old neonatal (G-I) wild-type HBV transgenic mouse liver DNA is shown.
Figure Legend Snippet: Tissue-specific and developmental regulation of HBV DNA methylation distribution. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from male (A-C) and female (D-F) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain DNA is shown. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from three independent 0.5 day old neonatal (G-I) wild-type HBV transgenic mouse liver DNA is shown.

Techniques Used: DNA Methylation Assay, Transgenic Assay

Effect of FoxA-deletion on HBV DNA methylation in adult mouse liver. The percentage of CpG DNA methylation at each position within the HBV genome from male (A) and female (B) FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The average percent methylation of the CpG sites spanning nucleotide coordinate 1–706 is correlated with the level of serum HBeAg.
Figure Legend Snippet: Effect of FoxA-deletion on HBV DNA methylation in adult mouse liver. The percentage of CpG DNA methylation at each position within the HBV genome from male (A) and female (B) FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The average percent methylation of the CpG sites spanning nucleotide coordinate 1–706 is correlated with the level of serum HBeAg.

Techniques Used: DNA Methylation Assay, Expressing, Transgenic Assay, Mouse Assay, Binding Assay, Methylation

Model for the tissue-specific and developmental regulation of HBV DNA methylation and transcription by the pioneer transcription factor, FoxA. (A) In the neonatal (P0.5) wild-type HBV transgenic mice, the HBV transgene DNA is extensively methylated but FoxA is expressed and marks the HBV genome for later developmental expression upon recruitment of additional transcription factors to the viral promoters. In the adult wild-type HBV transgenic mice, the HBV transgene DNA is unmethylated, FoxA plus additional transcription factors are recruited to the viral promoters and HBV RNA and DNA synthesis is observed. (B) In the neonatal (P0.5) FoxA-deficient HBV transgenic mice, the HBV transgene DNA is extensively methylated while limiting levels of FoxA fail to mark the HBV genome for later developmental DNA demethylation (due to the failure to recruit TET for active DNA demethylation and/or inhibition of DNA methylation during replication), and hence subsequent recruitment of additional transcription factors to the viral promoters with concomitant viral gene expression. In the adult FoxA-deficient HBV transgenic mice, the HBV genome remains extensively methylated because the limiting abundance of FoxA throughout development fails to mark the viral transgene DNA for demethylation which is essential for HBV RNA and DNA synthesis. (C) In the neonatal (P0.5) wild-type HBV transgenic mice, the essential liver-specific genes which are dependent on FoxA for their expression at this stage of development have presumably been marked by this pioneer transcription factor leading to the recruitment of additional transcription factors necessary for the demethylation and subsequent expression of these genes. Increasing levels of liver-specific transcription factors associated with liver maturation may be associated with increased levels of gene expression in the adult mice. (D) In contrast to the effect of limiting FoxA abundance on HBV DNA methylation and transcription, limiting postnatal FoxA abundance in the hepatocytes of these mice must be sufficient to support gene expression levels consistent with host viability presumably by marking these genes for DNA demethylation and transcription at the neonatal stage of development. The size of the transcription factors (FoxA and TFs) reflects the number of hepatocytes expressing HBV or essential liver-specific genes and/or the overall level of gene expression. The size of the arrow reflects the level of gene transcription. 5MeC, 5-methylcytosine; C, cytosine.
Figure Legend Snippet: Model for the tissue-specific and developmental regulation of HBV DNA methylation and transcription by the pioneer transcription factor, FoxA. (A) In the neonatal (P0.5) wild-type HBV transgenic mice, the HBV transgene DNA is extensively methylated but FoxA is expressed and marks the HBV genome for later developmental expression upon recruitment of additional transcription factors to the viral promoters. In the adult wild-type HBV transgenic mice, the HBV transgene DNA is unmethylated, FoxA plus additional transcription factors are recruited to the viral promoters and HBV RNA and DNA synthesis is observed. (B) In the neonatal (P0.5) FoxA-deficient HBV transgenic mice, the HBV transgene DNA is extensively methylated while limiting levels of FoxA fail to mark the HBV genome for later developmental DNA demethylation (due to the failure to recruit TET for active DNA demethylation and/or inhibition of DNA methylation during replication), and hence subsequent recruitment of additional transcription factors to the viral promoters with concomitant viral gene expression. In the adult FoxA-deficient HBV transgenic mice, the HBV genome remains extensively methylated because the limiting abundance of FoxA throughout development fails to mark the viral transgene DNA for demethylation which is essential for HBV RNA and DNA synthesis. (C) In the neonatal (P0.5) wild-type HBV transgenic mice, the essential liver-specific genes which are dependent on FoxA for their expression at this stage of development have presumably been marked by this pioneer transcription factor leading to the recruitment of additional transcription factors necessary for the demethylation and subsequent expression of these genes. Increasing levels of liver-specific transcription factors associated with liver maturation may be associated with increased levels of gene expression in the adult mice. (D) In contrast to the effect of limiting FoxA abundance on HBV DNA methylation and transcription, limiting postnatal FoxA abundance in the hepatocytes of these mice must be sufficient to support gene expression levels consistent with host viability presumably by marking these genes for DNA demethylation and transcription at the neonatal stage of development. The size of the transcription factors (FoxA and TFs) reflects the number of hepatocytes expressing HBV or essential liver-specific genes and/or the overall level of gene expression. The size of the arrow reflects the level of gene transcription. 5MeC, 5-methylcytosine; C, cytosine.

Techniques Used: DNA Methylation Assay, Transgenic Assay, Mouse Assay, Methylation, Expressing, DNA Synthesis, Inhibition

Related Articles

Amplification:

Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation
Article Snippet: .. The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument. .. Preparation of DNA for high-throughput amplicon sequencing was performed in two PCR steps in a protocol termed “targeted amplicon sequencing (TAS)” as described previously [ , ].

Article Title: New roles for DNA cytosine modification, eRNA, anchors, and superanchors in developing B cell progenitors
Article Snippet: .. Bisulfite-treated DNA was amplified by using a TruSeq PCR primer mixture and Pfu Turbo Cx Polymerase, agarose purified, and sequenced on an Illumina HiSEq 2000 sequencer. ..

Article Title: Reversal of Aberrant Cancer Methylome and Transcriptome upon Direct Reprogramming of Lung Cancer Cells
Article Snippet: .. Bisulfite-treated DNA was amplified and hybridized to the Infinium HumanMethylation27 BeadChip (Illumina), in accordance with the manufacturer's recommendations. ..

Article Title: Promoter Methylation in Head and Neck Squamous Cell Carcinoma Cell Lines Is Significantly Different than Methylation in Primary Tumors and Xenografts
Article Snippet: .. Bisulfite-treated DNA was amplified using primers designed using MethPrimer to span the sequence of the probes used on the Illumina Humanmethylation27 array. .. Array sequence data were obtained from the “Illumina Human Methylation Sequence Data.csv” file available for download at www.illumina.com .

Methylation:

Article Title: Quality Evaluation of Methyl Binding Domain Based Kits for Enrichment DNA-Methylation Sequencing
Article Snippet: .. Therefore, until further optimization of sequencing technologies allows for a cost-efficient whole-genome sequencing of bisulfite treated DNA or direct detection of methylated cytosines at base-resolution, MBD-seq might easily become the most widely used methodology. .. Lately, several commercial ‘DNA-methylation capturing’ kits for MBD-based affinity purification have been developed, typically with different options regarding salt concentration for the elution step.

Next-Generation Sequencing:

Article Title: Protocol for the study of cervical cancer screening technologies in HIV-infected women living in Rwanda
Article Snippet: .. Following bisulfite conversion and DNA purification and desulfonation, bisulfite-treated DNA will be used as template for Next-Gen Sequencing (NGS) (HiSeq2000, Illumina, San Diego, California, USA) using barcoded-type specific primers. ..

Purification:

Article Title: New roles for DNA cytosine modification, eRNA, anchors, and superanchors in developing B cell progenitors
Article Snippet: .. Bisulfite-treated DNA was amplified by using a TruSeq PCR primer mixture and Pfu Turbo Cx Polymerase, agarose purified, and sequenced on an Illumina HiSEq 2000 sequencer. ..

Real-time Polymerase Chain Reaction:

Article Title: DNA Methylation of the First Exon Is Tightly Linked to Transcriptional Silencing
Article Snippet: .. Bisulfite-treated DNA was analysed at selected genomic loci by quantitative PCR, Methylight , by deep sequencing using 454 Titanium Sequencer and by using the Illumina HumanMethylation27 microarray. .. Illumina arrays were processed as per manufacturer's instructions and data was extracted using BeadStudio software.

Sequencing:

Article Title: Quality Evaluation of Methyl Binding Domain Based Kits for Enrichment DNA-Methylation Sequencing
Article Snippet: .. Therefore, until further optimization of sequencing technologies allows for a cost-efficient whole-genome sequencing of bisulfite treated DNA or direct detection of methylated cytosines at base-resolution, MBD-seq might easily become the most widely used methodology. .. Lately, several commercial ‘DNA-methylation capturing’ kits for MBD-based affinity purification have been developed, typically with different options regarding salt concentration for the elution step.

Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation
Article Snippet: .. The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument. .. Preparation of DNA for high-throughput amplicon sequencing was performed in two PCR steps in a protocol termed “targeted amplicon sequencing (TAS)” as described previously [ , ].

Article Title: Protocol for the study of cervical cancer screening technologies in HIV-infected women living in Rwanda
Article Snippet: .. Following bisulfite conversion and DNA purification and desulfonation, bisulfite-treated DNA will be used as template for Next-Gen Sequencing (NGS) (HiSeq2000, Illumina, San Diego, California, USA) using barcoded-type specific primers. ..

Article Title: DNA Methylation of the First Exon Is Tightly Linked to Transcriptional Silencing
Article Snippet: .. Bisulfite-treated DNA was analysed at selected genomic loci by quantitative PCR, Methylight , by deep sequencing using 454 Titanium Sequencer and by using the Illumina HumanMethylation27 microarray. .. Illumina arrays were processed as per manufacturer's instructions and data was extracted using BeadStudio software.

Article Title: Promoter Methylation in Head and Neck Squamous Cell Carcinoma Cell Lines Is Significantly Different than Methylation in Primary Tumors and Xenografts
Article Snippet: .. Bisulfite-treated DNA was amplified using primers designed using MethPrimer to span the sequence of the probes used on the Illumina Humanmethylation27 array. .. Array sequence data were obtained from the “Illumina Human Methylation Sequence Data.csv” file available for download at www.illumina.com .

DNA Purification:

Article Title: Protocol for the study of cervical cancer screening technologies in HIV-infected women living in Rwanda
Article Snippet: .. Following bisulfite conversion and DNA purification and desulfonation, bisulfite-treated DNA will be used as template for Next-Gen Sequencing (NGS) (HiSeq2000, Illumina, San Diego, California, USA) using barcoded-type specific primers. ..

Genome Wide:

Article Title: Differential epigenetic and transcriptional response of the skeletal muscle carnitine palmitoyltransferase 1B (CPT1B) gene to lipid exposure with obesity
Article Snippet: .. Genome-wide DNA methylation analysis was conducted on bisulfite-treated DNA samples using the Illumina Infinium HumanMethylation 450K BeadChip, which allows the quantitative monitoring of 485,764 cytosine positions ( ). .. Twelve micriliters of each bisulfite-converted sample was amplified and fragmented, following the manufacturer's protocol, hybridized to arrays in a balanced design, and scanned on an Illumina iScan System.

Polymerase Chain Reaction:

Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation
Article Snippet: .. The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument. .. Preparation of DNA for high-throughput amplicon sequencing was performed in two PCR steps in a protocol termed “targeted amplicon sequencing (TAS)” as described previously [ , ].

Article Title: New roles for DNA cytosine modification, eRNA, anchors, and superanchors in developing B cell progenitors
Article Snippet: .. Bisulfite-treated DNA was amplified by using a TruSeq PCR primer mixture and Pfu Turbo Cx Polymerase, agarose purified, and sequenced on an Illumina HiSEq 2000 sequencer. ..

DNA Methylation Assay:

Article Title: Differential epigenetic and transcriptional response of the skeletal muscle carnitine palmitoyltransferase 1B (CPT1B) gene to lipid exposure with obesity
Article Snippet: .. Genome-wide DNA methylation analysis was conducted on bisulfite-treated DNA samples using the Illumina Infinium HumanMethylation 450K BeadChip, which allows the quantitative monitoring of 485,764 cytosine positions ( ). .. Twelve micriliters of each bisulfite-converted sample was amplified and fragmented, following the manufacturer's protocol, hybridized to arrays in a balanced design, and scanned on an Illumina iScan System.

Microarray:

Article Title: DNA Methylation of the First Exon Is Tightly Linked to Transcriptional Silencing
Article Snippet: .. Bisulfite-treated DNA was analysed at selected genomic loci by quantitative PCR, Methylight , by deep sequencing using 454 Titanium Sequencer and by using the Illumina HumanMethylation27 microarray. .. Illumina arrays were processed as per manufacturer's instructions and data was extracted using BeadStudio software.

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    Illumina Inc bisulphite treated dna
    <t>DNA</t> methylation at the sentinel CpG sites in whole blood and in 4 isolated cell subsets (Monocytes, Neutrophils, CD4+, CD8+) from 60 individuals (30 obese cases, and 30 normal weight controls) by <t>Illumina</t> MethylationEPIC array, which quantifies 179 of the 187 sentinel markers. Results are shown as a heatmap, coded by methylation value (hypomethylation
    Bisulphite Treated Dna, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 90/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bisulphite treated dna/product/Illumina Inc
    Average 90 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    bisulphite treated dna - by Bioz Stars, 2020-07
    90/100 stars
      Buy from Supplier

    93
    Illumina Inc bisulfite treated dna
    Effect of FoxA-deletion on <t>HBV</t> <t>DNA</t> methylation distribution in adult mouse liver. The CpG DNA methylation frequency distribution across the 11, 38 and 14 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2131–2441, respectively, from male (A, C and E) and female (B, D and F) FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-); M A1A2A3Cre(-) and F A1A2A3Cre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+); M A1A2A3Cre(+) and F A1A2A3Cre(+)) HBV transgenic mice is shown.
    Bisulfite Treated Dna, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 93/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bisulfite treated dna/product/Illumina Inc
    Average 93 stars, based on 28 article reviews
    Price from $9.99 to $1999.99
    bisulfite treated dna - by Bioz Stars, 2020-07
    93/100 stars
      Buy from Supplier

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    DNA methylation at the sentinel CpG sites in whole blood and in 4 isolated cell subsets (Monocytes, Neutrophils, CD4+, CD8+) from 60 individuals (30 obese cases, and 30 normal weight controls) by Illumina MethylationEPIC array, which quantifies 179 of the 187 sentinel markers. Results are shown as a heatmap, coded by methylation value (hypomethylation

    Journal: Nature

    Article Title: Epigenome-wide association study of body mass index, and the adverse outcomes of adiposity

    doi: 10.1038/nature20784

    Figure Lengend Snippet: DNA methylation at the sentinel CpG sites in whole blood and in 4 isolated cell subsets (Monocytes, Neutrophils, CD4+, CD8+) from 60 individuals (30 obese cases, and 30 normal weight controls) by Illumina MethylationEPIC array, which quantifies 179 of the 187 sentinel markers. Results are shown as a heatmap, coded by methylation value (hypomethylation

    Article Snippet: Methylation analysis of the bisulphite-treated DNA was performed using Illumina Infinium MethylationEPIC Beadchip (Illumina, San Diego, CA) according to standard protocol.

    Techniques: DNA Methylation Assay, Isolation, Methylation

    Study design. Epigenome-wide association and replication testing was performed in order to identify methylation sites associated with adiposity. In the discovery step, four large cohorts were included with Illumina 450k DNA methylation data available, which were preprocessed and quality controlled according to a harmonized protocol. Epigenome-wide association was performed in every single study with BMI as response variable and methylation β-value as independent variable, adjusting for covariates as described in the Online Methods . At a genome-wide significance level of P

    Journal: Nature

    Article Title: Epigenome-wide association study of body mass index, and the adverse outcomes of adiposity

    doi: 10.1038/nature20784

    Figure Lengend Snippet: Study design. Epigenome-wide association and replication testing was performed in order to identify methylation sites associated with adiposity. In the discovery step, four large cohorts were included with Illumina 450k DNA methylation data available, which were preprocessed and quality controlled according to a harmonized protocol. Epigenome-wide association was performed in every single study with BMI as response variable and methylation β-value as independent variable, adjusting for covariates as described in the Online Methods . At a genome-wide significance level of P

    Article Snippet: Methylation analysis of the bisulphite-treated DNA was performed using Illumina Infinium MethylationEPIC Beadchip (Illumina, San Diego, CA) according to standard protocol.

    Techniques: Methylation, DNA Methylation Assay, Genome Wide

    Distribution of methylation-phenotype associations. Distribution of −log 10 p -values for bootstrap analysis of BMI and DNA methylation in cord blood DNA according to mean methylation levels at the 44 CpG sites analysed.

    Journal: PLoS ONE

    Article Title: DNA Methylation Patterns in Cord Blood DNA and Body Size in Childhood

    doi: 10.1371/journal.pone.0031821

    Figure Lengend Snippet: Distribution of methylation-phenotype associations. Distribution of −log 10 p -values for bootstrap analysis of BMI and DNA methylation in cord blood DNA according to mean methylation levels at the 44 CpG sites analysed.

    Article Snippet: Site-specific CpG methylation was analysed using 5 µl (at 50 ng/µl) bisulphite treated DNA using the GoldenGate® Cancer Panel I Array (Illumina Inc, USA) and the GoldenGate® Assay Kit with UDG on the Sentrix Universal-96 Array matrix v7A.

    Techniques: Methylation, DNA Methylation Assay

    Effect of FoxA-deletion on HBV DNA methylation distribution in adult mouse liver. The CpG DNA methylation frequency distribution across the 11, 38 and 14 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2131–2441, respectively, from male (A, C and E) and female (B, D and F) FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-); M A1A2A3Cre(-) and F A1A2A3Cre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+); M A1A2A3Cre(+) and F A1A2A3Cre(+)) HBV transgenic mice is shown.

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: Effect of FoxA-deletion on HBV DNA methylation distribution in adult mouse liver. The CpG DNA methylation frequency distribution across the 11, 38 and 14 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2131–2441, respectively, from male (A, C and E) and female (B, D and F) FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-); M A1A2A3Cre(-) and F A1A2A3Cre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+); M A1A2A3Cre(+) and F A1A2A3Cre(+)) HBV transgenic mice is shown.

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: DNA Methylation Assay, Expressing, Transgenic Assay, Mouse Assay

    RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of 1, 2, 3, 4 and 7 week old HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A1A2A3). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. The levels of the transcripts which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of 1, 2, 3, 4 and 7 week old HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A1A2A3). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. The levels of the transcripts which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: Northern Blot, Hybridization, Quantitative RT-PCR, Transgenic Assay, Mouse Assay, Expressing, Quantitation Assay

    RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of adult HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. Average number of mice per group was 6.6±1.9 (Range: 4–9). The levels of the HBV 3.5kb transcript which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: RNA (Northern) filter hybridization and RT-qPCR analysis of HBV transcripts in the livers of adult HBV transgenic mice. (A) RNA (Northern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probes used were HBV ayw genomic DNA plus GAPDH cDNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) transcript was used as an internal control for the quantitation of the HBV 3.5kb RNA. (B) Quantitative analysis by RNA (Northern) filter hybridization of the HBV 3.5kb transcript in the HBV transgenic mice. The mean HBV 3.5kb transcript levels plus standard deviations are indicated. Average number of mice per group was 6.6±1.9 (Range: 4–9). The levels of the HBV 3.5kb transcript which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: Northern Blot, Hybridization, Quantitative RT-PCR, Transgenic Assay, Mouse Assay, Expressing, Quantitation Assay

    Tissue-specific and developmental regulation of HBV DNA methylation. (A) The percentage of CpG DNA methylation at each position within the HBV genome from a male (A) and female (B) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The percentage of CpG DNA methylation at each position within the HBV genome from three individual 0.5 day old neonatal wild-type HBV transgenic mouse livers is shown.

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: Tissue-specific and developmental regulation of HBV DNA methylation. (A) The percentage of CpG DNA methylation at each position within the HBV genome from a male (A) and female (B) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The percentage of CpG DNA methylation at each position within the HBV genome from three individual 0.5 day old neonatal wild-type HBV transgenic mouse livers is shown.

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: DNA Methylation Assay, Transgenic Assay, Binding Assay

    DNA (Southern) filter hybridization analysis of HBV DNA replication intermediates in the livers of adult HBV transgenic mice. (A) DNA (Southern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probe used was HBVayw genomic DNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The HBV transgene (Tg) was used as an internal control for the quantitation of the HBV replication intermediates. Tg = HBV transgene; RC = HBV relaxed circular replication intermediates; SS = HBV single stranded replication intermediates. (B) Quantitative analysis of the HBV DNA replication intermediate (RI) levels in HBV transgenic mice. The mean DNA replication intermediate levels plus standard deviations are indicated. Average number of mice per group was 6.7±1.8 (Range: 4–9). The levels of replication intermediates which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: DNA (Southern) filter hybridization analysis of HBV DNA replication intermediates in the livers of adult HBV transgenic mice. (A) DNA (Southern) filter hybridization analysis of representative mice of each sex and genotype are shown. Noncontiguous lanes from multiple analysis are presented. The probe used was HBVayw genomic DNA. FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice are indicated (Genotype A2, A1A2 and A1A2A3, respectively). The HBV transgene (Tg) was used as an internal control for the quantitation of the HBV replication intermediates. Tg = HBV transgene; RC = HBV relaxed circular replication intermediates; SS = HBV single stranded replication intermediates. (B) Quantitative analysis of the HBV DNA replication intermediate (RI) levels in HBV transgenic mice. The mean DNA replication intermediate levels plus standard deviations are indicated. Average number of mice per group was 6.7±1.8 (Range: 4–9). The levels of replication intermediates which are statistically significantly different between Cre(-) and Cre(+) HBV transgenic mice by a Student’s t-test (p

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: Hybridization, Transgenic Assay, Mouse Assay, Expressing, Quantitation Assay

    Tissue-specific and developmental regulation of HBV DNA methylation distribution. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from male (A-C) and female (D-F) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain DNA is shown. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from three independent 0.5 day old neonatal (G-I) wild-type HBV transgenic mouse liver DNA is shown.

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: Tissue-specific and developmental regulation of HBV DNA methylation distribution. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from male (A-C) and female (D-F) wild-type HBV transgenic mouse liver, kidney, muscle, spleen, lung and brain DNA is shown. The CpG DNA methylation frequency distribution across the 11, 38 and 13 sites within HBV nucleotide coordinates 341–711, 1215–1629 and 2264–2474, respectively, from three independent 0.5 day old neonatal (G-I) wild-type HBV transgenic mouse liver DNA is shown.

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: DNA Methylation Assay, Transgenic Assay

    Effect of FoxA-deletion on HBV DNA methylation in adult mouse liver. The percentage of CpG DNA methylation at each position within the HBV genome from male (A) and female (B) FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The average percent methylation of the CpG sites spanning nucleotide coordinate 1–706 is correlated with the level of serum HBeAg.

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: Effect of FoxA-deletion on HBV DNA methylation in adult mouse liver. The percentage of CpG DNA methylation at each position within the HBV genome from male (A) and female (B) FoxA-expressing (HBVFoxA2 fl/fl AlbCre(-), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(-) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(-)) and FoxA-deleted (HBVFoxA2 fl/fl AlbCre(+), HBVFoxA1 fl/fl FoxA2 fl/fl AlbCre(+) and HBVFoxA1 fl/fl FoxA2 fl/fl FoxA3 +/- AlbCre(+)) HBV transgenic mice is shown. The positions of the viral transcription initiation sites for the X-gene (X RNA), the precore/pregenomic transcripts (C RNA), the large surface antigen transcript (PS RNA) and the middle/major surface antigen transcript (S RNA) are shown. The locations of the FoxA binding sites and CpG island within the HBV genome are also indicated. (C) The average percent methylation of the CpG sites spanning nucleotide coordinate 1–706 is correlated with the level of serum HBeAg.

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: DNA Methylation Assay, Expressing, Transgenic Assay, Mouse Assay, Binding Assay, Methylation

    Model for the tissue-specific and developmental regulation of HBV DNA methylation and transcription by the pioneer transcription factor, FoxA. (A) In the neonatal (P0.5) wild-type HBV transgenic mice, the HBV transgene DNA is extensively methylated but FoxA is expressed and marks the HBV genome for later developmental expression upon recruitment of additional transcription factors to the viral promoters. In the adult wild-type HBV transgenic mice, the HBV transgene DNA is unmethylated, FoxA plus additional transcription factors are recruited to the viral promoters and HBV RNA and DNA synthesis is observed. (B) In the neonatal (P0.5) FoxA-deficient HBV transgenic mice, the HBV transgene DNA is extensively methylated while limiting levels of FoxA fail to mark the HBV genome for later developmental DNA demethylation (due to the failure to recruit TET for active DNA demethylation and/or inhibition of DNA methylation during replication), and hence subsequent recruitment of additional transcription factors to the viral promoters with concomitant viral gene expression. In the adult FoxA-deficient HBV transgenic mice, the HBV genome remains extensively methylated because the limiting abundance of FoxA throughout development fails to mark the viral transgene DNA for demethylation which is essential for HBV RNA and DNA synthesis. (C) In the neonatal (P0.5) wild-type HBV transgenic mice, the essential liver-specific genes which are dependent on FoxA for their expression at this stage of development have presumably been marked by this pioneer transcription factor leading to the recruitment of additional transcription factors necessary for the demethylation and subsequent expression of these genes. Increasing levels of liver-specific transcription factors associated with liver maturation may be associated with increased levels of gene expression in the adult mice. (D) In contrast to the effect of limiting FoxA abundance on HBV DNA methylation and transcription, limiting postnatal FoxA abundance in the hepatocytes of these mice must be sufficient to support gene expression levels consistent with host viability presumably by marking these genes for DNA demethylation and transcription at the neonatal stage of development. The size of the transcription factors (FoxA and TFs) reflects the number of hepatocytes expressing HBV or essential liver-specific genes and/or the overall level of gene expression. The size of the arrow reflects the level of gene transcription. 5MeC, 5-methylcytosine; C, cytosine.

    Journal: PLoS Pathogens

    Article Title: Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation

    doi: 10.1371/journal.ppat.1006239

    Figure Lengend Snippet: Model for the tissue-specific and developmental regulation of HBV DNA methylation and transcription by the pioneer transcription factor, FoxA. (A) In the neonatal (P0.5) wild-type HBV transgenic mice, the HBV transgene DNA is extensively methylated but FoxA is expressed and marks the HBV genome for later developmental expression upon recruitment of additional transcription factors to the viral promoters. In the adult wild-type HBV transgenic mice, the HBV transgene DNA is unmethylated, FoxA plus additional transcription factors are recruited to the viral promoters and HBV RNA and DNA synthesis is observed. (B) In the neonatal (P0.5) FoxA-deficient HBV transgenic mice, the HBV transgene DNA is extensively methylated while limiting levels of FoxA fail to mark the HBV genome for later developmental DNA demethylation (due to the failure to recruit TET for active DNA demethylation and/or inhibition of DNA methylation during replication), and hence subsequent recruitment of additional transcription factors to the viral promoters with concomitant viral gene expression. In the adult FoxA-deficient HBV transgenic mice, the HBV genome remains extensively methylated because the limiting abundance of FoxA throughout development fails to mark the viral transgene DNA for demethylation which is essential for HBV RNA and DNA synthesis. (C) In the neonatal (P0.5) wild-type HBV transgenic mice, the essential liver-specific genes which are dependent on FoxA for their expression at this stage of development have presumably been marked by this pioneer transcription factor leading to the recruitment of additional transcription factors necessary for the demethylation and subsequent expression of these genes. Increasing levels of liver-specific transcription factors associated with liver maturation may be associated with increased levels of gene expression in the adult mice. (D) In contrast to the effect of limiting FoxA abundance on HBV DNA methylation and transcription, limiting postnatal FoxA abundance in the hepatocytes of these mice must be sufficient to support gene expression levels consistent with host viability presumably by marking these genes for DNA demethylation and transcription at the neonatal stage of development. The size of the transcription factors (FoxA and TFs) reflects the number of hepatocytes expressing HBV or essential liver-specific genes and/or the overall level of gene expression. The size of the arrow reflects the level of gene transcription. 5MeC, 5-methylcytosine; C, cytosine.

    Article Snippet: The 99 CpG sequences in the HBV DNA genome were targeted using PCR amplification of the bisulfite-treated DNA, followed by sequencing of the amplicons on an Illumina MiSeq instrument.

    Techniques: DNA Methylation Assay, Transgenic Assay, Mouse Assay, Methylation, Expressing, DNA Synthesis, Inhibition