Open Access Research article

Nuclear Factor I genomic binding associates with chromatin boundaries

Milos Pjanic1*, Christoph D Schmid25, Armelle Gaussin16, Giovanna Ambrosini2, Jozef Adamcik37, Petar Pjanic4, Genta Plasari18, Jan Kerschgens1, Giovani Dietler3, Philipp Bucher2 and Nicolas Mermod1

Author Affiliations

1 Institute of Biotechnology and Center for Biotecghnology UNIL-EPFL, University of Lausanne, Lausanne, 1015, Switzerland

2 Ecole Polytechnique Fédérale de Lausanne and Swiss Institute of Bioinformatics, Lausanne, 1015, Switzerland

3 Laboratory of Physics of Living Matter, Ecole Polytechnique Fédérale de Lausanne, Lausanne, 1015, Switzerland

4 Peripheral Systems Laboratory, Ecole polytechnique Fédérale de Lausanne, Lausanne, 1015, Switzerland

5 Present address: Swiss Tropical and Public Health Institute and University of Basel, Basel, Switzerland

6 Present address: Selexis SA, Geneva, Switzerland

7 Present address: ETH Zurich, Department of Health Science and Technology, Zurich, Switzerland

8 Present address: Regenlab SA, Mont-sur-Lausanne, Switzerland

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BMC Genomics 2013, 14:99  doi:10.1186/1471-2164-14-99

Published: 12 February 2013

Additional files

Additional file 1: Figure S1:

Number of predicted genomic NFI binding sites as a function of the position weight matrix score threshold. Figure S2. NFI predicted sites in the vicinity of in vivo occupied sites - effect of different tag threshold values for defining in vivo binding sites. Figure S3. NFI ChIP-Seq tags preferentially map to the vicinity of NFI predicted sites – effect of lowering the weight matrix score cut-off. Figure S4. Comparison of ChiP-Peak and MACS algorithms for peak calling in ChIP-Seq experiments. Figure S5. Tags mapping on plus and minus strands are symmetrically distributed around NFI predicted sites. Figure S6. Sequence analysis of NFI in vivo sites from wild-type and knock out mouse embryonic fibroblasts. Figure S7. NFI-C knock-out mouse embryonic fibroblasts show reduction in NFI protein levels and occupancy of predicted sites. Figure S8. Positional correlation between plus and minus tags corresponds to the NFI –DNA complex length. Figure S9. Positional correlation of tags mapping on plus and minus strand from unprecipitated control dataset. Figure S10. Atomic force microscopy assay of the length of DNA fragments generated by the sonication of crosslinked chromatin. Figure S11. Proposed mode of interaction of NFI and nucleosomal particles based on the ChIP-Seq analysis. Figure S12. NFI in vivo-occupied sites at miRNA TSS colocalize with H3K4Me3 and H3K36me3 modifications. Figure S13. Distribution of distances from histone modification boundaries to the closest NFI or randomly selected site. Figure S14. NFI in vivo sites are often located near chromatin domain boundaries. Figure S15. NFI predicted sites are more frequently occupied at NFI-C up-regulated genes. Figure S16. Average ChIP DNA fragment length submitted for sequencing with the Illumina Genome Analyzer.

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Additional file 2: Table S1:

DNA motifs found with the program peak-motifs in peak lists obtained with different tag thresholds. Table S2. Distribution of in vivo and matrix-predicted NFI sites on the mouse genome. Table S3. Distribution of NFI in vivo sites surrounding miRNA loci. Table S4. Predicted and occupied site distribution at NFI-C-regulated and non-regulated genes.

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