Genome-wide analysis of Fis binding in Escherichia coli indicates a causative role for A-/AT-tracts.

TitleGenome-wide analysis of Fis binding in Escherichia coli indicates a causative role for A-/AT-tracts.
Publication TypeJournal Article
Year of Publication2008
AuthorsCho B-K, Knight EM, Barrett CL, Palsson BØ
JournalGenome research
PubMed Date2008 Jun
KeywordsAdenine, AT Rich Sequence, Binding Sites, Chromosome Mapping, DNA, Bacterial, DNA-Directed RNA Polymerases, Escherichia coli, Escherichia coli Proteins, Factor For Inversion Stimulation Protein, Gene Deletion, Genome, Bacterial, Immunoprecipitation, Sigma Factor, Thymine, Transcription, Genetic

We determined the genome-wide distribution of the nucleoid-associated protein Fis in Escherichia coli using chromatin immunoprecipitation coupled with high-resolution whole genome-tiling microarrays. We identified 894 Fis-associated regions across the E. coli genome. A significant number of these binding sites were found within open reading frames (33%) and between divergently transcribed transcripts (5%). Analysis indicates that A-tracts and AT-tracts are an important signal for preferred Fis-binding sites, and that A(6)-tracts in particular constitute a high-affinity signal that dictates Fis phasing in stretches of DNA containing multiple and variably spaced A-tracts and AT-tracts. Furthermore, we find evidence for an average of two Fis-binding regions per supercoiling domain in the chromosome of exponentially growing cells. Transcriptome analysis shows that approximately 21% of genes are affected by the deletion of fis; however, the changes in magnitude are small. To address the differential Fis bindings under growth environment perturbation, ChIP-chip analysis was performed using cells grown under aerobic and anaerobic growth conditions. Interestingly, the Fis-binding regions are almost identical in aerobic and anaerobic growth conditions-indicating that the E. coli genome topology mediated by Fis is superficially identical in the two conditions. These novel results provide new insight into how Fis modulates DNA topology at a genome scale and thus advance our understanding of the architectural bases of the E. coli nucleoid.

Alternate JournalGenome Res.
PubMed ID18340041



417 Powell-Focht Bioengineering Hall

9500 Gilman Drive La Jolla, CA 92093-0412

Contact Us

Contact Us

In Silico Lab:  858-822-1144

Wet Lab:  858-246-1625

FAX:   858-822-3120

Website Concerns:


Visit the Official SBRG YouTube Channel

User Login