IPOD-HR, ChIP-seq, RNA-seq of E. coli nucleoid associated protein deletions

There is increasing evidence that microbes maintain a structured chromosome, which in turn impacts gene expression. However tools to profile the genome landscape and binding of key architectural proteins have been limited. We recently discovered densely occupied, multi-kilobase regions in E. coli that are transcriptionally silent, similar to eukaryotic heterochromatin. These regions, termed EPODs, overlap metabolic pathways and parasitic elements such as prophages. Here, we investigate the contributions of nucleoid associated proteins (NAPs) to these domains by examining the impacts of deleting NAPs on EPODs genome-wide in E. coli and an evolutionarily distant species, Bacillus subtilis. We identify key NAPs contributing to the silencing of specific EPODs, where deletion of a particular NAPs opens a chromosomal region to RNA polymerase binding. In E. coli, we distinguish novel xenogeneic silencing NAPs, Fis and Hfq, that are essential for cell viability in the presence of domesticated prophages. Furthermore, we show that changes in EPODs facilitate an extra layer of transcriptional regulation to prepare cells for exposure to exotic carbon sources. Our findings demonstrate a new suite of mechanisms through which genomic architecture primes bacteria for changing metabolic environments and silences harmful genomic elements Overall design: IPOD-HR, ChIP-seq, RNA-seq of E. coli nucleoid associated protein deletions Please note that the processed data for the RNA-seq samples have been replaced and the data processing description has been updated on 12/28/2021.