Disease relevance of ftsK

• A mutation in the ftsK gene of Escherichia coli affects cell-cell separation, stationary-phase survival, stress adaptation, and expression of the gene encoding the stress protein UspA [1].

High impact information on ftsK

• Chromosome dimers, which frequently form in Escherichia coli, are resolved by the combined action of two tyrosine recombinases, XerC and XerD, acting at a specific site on the chromosome, dif, together with the cell division protein FtsK [2].
• Analysis of molecular diffusion in ftsK cell-division mutants using laser surgery [3].
• Rather, this mutation acts as a general suppressor of division defects, which include deletions of the normally essential genes zipA and ftsK and mutations in FtsQ that affect both localization and recruitment [4].
• In contrast, the 5' end of the ftsK locus reported to complement ftsK44(Ts) phenotypes does not complement the phenotypes of the ftsK1::cat mutant [1].
• In addition, plasmids harboring a truncated ftsK allele lacking the last 195 bp of the gene cause chain formation in wild-type cells [1].

Biological context of ftsK

• The phenotypes of the ftsK1::cat mutant are complemented by the 3' end (spoIIIE-like half) of the ftsK locus [1].

References