@article {Falconi:1993:0950-382X:273,
title = "Expression of the gene encoding the major bacterial nucleoid protein HNS is subject to transcriptional autorepression",
journal = "Molecular Microbiology",
parent_itemid = "infobike://bsc/mole",
publishercode ="bp",
year = "1993",
volume = "10",
number = "2",
publication date ="1993-10-01T00:00:00",
pages = "273-282",
itemtype = "ARTICLE",
issn = "0950-382X",
eissn = "1365-2958",
url = "https://www.ingentaconnect.com/content/bsc/mole/1993/00000010/00000002/art00007",
doi = "doi:10.1111/j.1365-2958.1993.tb01953.x",
author = "Falconi, Maurizio and Higgins, N. Patrick and Spurio, Roberto and Pon, Cynthia L. and Gualerzi, Claudio O.",
abstract = "Summary Expression of a promoterless cat gene fused to a DNA fragment of approximately 400 bp, beginning at 313 of Escherichia coli hns, was significantly repressed in E. coli and Salmonella typhimurium strains
with wildtype hns but not in mutants carrying hns alleles. CAT expression from fusions containing a shorter (110 bp) segment of hns was essentially unaffected in the same genetic backgrounds. The stage of growth was found to influence the extent of repression which
was maximum (approximately 75%) in midlog cultures and negligible in cells entering the stationary phase. The level of repression in earlylog phase was lower than in midlog phase cultures, probably because of the presence of high levels of Fis protein, which counteracts
the HNS inhibition by stimulating hns transcription. The effects observed in vivo were mirrored by similar results obtained in vitro upon addition of purified HNS and Fis protein to transcriptional systems programmed with the same hns caf fusions.
Electrophoretic gel shift assays, DNase I footprinting and cyclic permutation get analyses revealed that HNS binds preferentially to the upstream region of its own gene recognizing two rather extended segments of DNA on both sides of a bend centred around 150. When these sites
are filled by HNS, an additional site between approximately 20 and 65, which partly overlaps the promoter, is also occupied. Binding of HNS to this site is probably the ultimate cause of transcriptional autorepression.",
}