Project description:We mapped the genome-wide binding of the flagellar regulators FlhD, FlhC, and FliA in FLAG-tagged derivatives of E. coli K-12 MG1655 using ChIP coupled with deep sequencing (ChIP-seq). We identify new binding sites for each factor.
Project description:We mapped the genome-wide binding of C-terminally FLAG-tagged AraC in S. enterica subsp. enterica serovar Typhimurium strain 14028s using ChIP coupled with deep sequencing (ChIP-seq). We identified five putative target loci for AraC: upstream of araB/araC, araE, araJ, STM14_0178, and within sseD.
Project description:We mapped the genome-wide binding of sigma 70 in E. coli K-12 MG1655 and an hns mutant that is otherwise isogenic using ChIP coupled with deep sequencing (ChIP-seq). We show that intragenic binding of sigma 70 is increased in the hns mutant.
Project description:We used ChIP-seq to map binding of the CRISPR surveillance complex, Cascade, in a Salmonella enterica serovar Typhimurium strain lacking the gene encoding the endonuclease Cas3. We performed ChIP-seq in strains with wild-type and mutant sequences upstream of the two CRISPR arrays, and in strains with wild-type and mutant nusE genes to determine the impact of Nus factor antitermination on CRISPR array function.
Project description:To determine sites where RpoS binds (and hence likely plays a direct role in transcription), we used ChIP-seq to map the association of RpoS across the Escherichia coli chromosome during stationary phase growth in minimal medium. To facilitate ChIP, RpoS was C-terminally SPA-tagged at its native locus.
Project description:We used ChIP-seq to map binding of the CRISPR surveillance complex, Cascade, in an E. coli strain lacking the endonuclease Cas3. These data enabled us to determine the precise sequence requirements for Cascade binding.
Project description:To generate and compile data from ChIP-Seq libraries. Looking at genome-wide binding of transcription factors HilD, HilC, RtsA, RtsB, SprB, and InvF under SPI-1 inducing growth conditions in duplicate.
Project description:Disrupted in schizophrenia 1 (DISC1) has been implicated in contributing to a number of psychiatric diseases and neurodevelopmental phenotypes such as the proliferation and differentiation of neural progenitor cells. While there has been significant effort directed towards understanding the function of DISC1 through the determination of its protein-protein interactions within an in-vitro setting, endogenous interactions involving DISC1 within a cell-type specific setting relevant to neural development remain unclear.