Disease relevance of kilR

• Identification of a new inhibitor of essential division gene ftsZ as the kil gene of defective prophage Rac [1].
• Broad host range plasmid RK2 encodes multiple kil genes potentially lethal to Escherichia coli host cells [2].
• The kil gene of bacteriophage lambda [3].
• The Tn5-based transposon Tn5-KIL3 (Miksch et al. 1997c) bearing the kil gene of the ColE1 plasmid of Escherichia coli, which mediates controlled export of periplasmic proteins into the culture medium, was stably integrated into the chromosome of Klebsiella planticola with high transposition frequency [4].
• Controlled secretion into the culture medium of a hybrid beta-glucanase by Acetobacter methanolicus mediated by the kil gene of Escherichia coli located on a Tn5-derived transposon [5].

High impact information on kilR

• The kil and kor genes are located in four distinct regions of the RK2 genome [2].
• The three promoter regions share common palindromic sequences which may serve as sites for the coordinate regulation of replication and kil functions [6].
• The cell division block is a result of the transient expression of the lambda kil gene [7].
• Two peptides that could be respectively precursor and mature products of colicin E1 kil gene were detected on an SDS/polyacrylamide gel [8].
• The kil gene was shown to cause cell death and filamentation as described previously [9].

Chemical compound and disease context of kilR

• The lambda kil gene has been shown to be responsible for premature lysis effected by addition of chloramphenicol between 15 and 20 min after thermal induction of a lambda prophage [10].
• This transposon contained the kil gene of the ColEl plasmid under the growth-phase-dependent promoter of the fic gene (filamentation induced by cAMP) of Escherichia coli, an interposon located upstream of kil, a kanamycin/neomycin-resistance gene, a multiple cloning site and the mob site [5].

Biological context of kilR

• The kil gene product acts independently of the min operon, and its effects are increased in conditions of high cyclic AMP (cAMP) receptor protein-cAMP complex levels in the cell [1].
• This indicates that in these mutants the various effects of kil gene expression have become dissociated [11].
• Cold-sensitive phenotype of Escherichia coli cells harboring a plasmid carrying the kil gene of phage lambda brought under control of cI857 gene promoters [12].
• Here, we localized the kil reading frame [10].
• We report the identification of two nested genes, kil and eta, located in the P4 left operon [13].

Anatomical context of kilR

• Expression of the plasmid-borne kil gene resulted in growth arrest, a reduction of colony-forming units and filament formation [10].
• The protein pattern of periplasm and culture medium was analyzed before and after induction of the kil gene expression, indicating that the release of periplasmic proteins is semiselective [14].
• The kil peptide induces the secretion of homologous or heterologous proteins in two steps, first acting on the cytoplasmic membrane, then permeabilizing the outer membrane [15].

Regulatory relationships of kilR

• When controlled by the fic promoter, the kil gene led to a higher total production of beta-glucanase and a higher protein secretion than when it was under control of the bolA promoter [16].

Other interactions of kilR

• These features distinguish kil-encoded protein from the inhibitory product of gene dicB, which occupies a similar genetic location in Kim (Qin), another defective prophage of Escherichia coli [1].
• The kil gene was fused with the stationary-phase promoter of the fic gene of E. coli, and a secretion cassette (Kil-Km cassette) containing the regulated kil gene, the Km-resistance gene, and multiple cloning sites for the integration of target genes was constructed [14].

References