Disease relevance of seqA

• Dam-dependent phase variation of Ag43 in Escherichia coli is altered in a seqA mutant [1].
• In addition to transcripts about 300 nucleotides long, P4 prophage produces a family of shorter transcripts, about 80 nucleotides long, containing seqA or seqB [2].
• Genetic analysis demonstrated that CII-mediated activation of the phage pI and paQ promoters, which are required for efficient lysogenization, is less efficient in the absence of seqA function [3].
• Interestingly, seqA is only present in a few DamMT-specifying proteobacteria [4].
• Null mutation of the dam or seqA gene suppresses temperature-sensitive lethality but not hypersensitivity to novobiocin of muk null mutants [5].

High impact information on seqA

• In contrast to wild-type and dnaA(Ts) cells, seqA mutant cells frequently go through two initiation events per cell division cycle, and all the origins present in each cell are not initiated in synchrony [6].
• In part, this can be attributed to the observed decrease in the level of DNA methylation in the seqA mutant [1].
• The amounts of the intercalative agent required to relax the supercoiled chromosome in mukB and seqA mutants were lower and higher, respectively, than for the wild-type parent, confirming that these cell cycle genes modulate the topology of the E. coli chromosome [7].
• We have used ethidium bromide titration for direct measurement of the changes in the negative supercoiling of Escherichia coli chromosome caused by mutations inactivating the cell cycle functions mukB and seqA [7].
• Increasing DnaA activity in a strain capable of suppression, by introducing a copy of the wild-type allele, increasing the suppressor gene dosage or introducing a seqA mutation, reversed the suppression [8].

Biological context of seqA

• Both seqA and seqC single mutants were still sensitive to P4 prophage immunity, whereas P4 seqA seqC double mutants showed a virulent phenotype [9].
• Mutations in either seqA or seqC that alter its complementarity to seqB abolished or reduced P4 lysogenization proficiency and delayed the shutoff of the long transcripts originating from PLE that cover the entire operon [9].
• However, the asynchronous initiation of chromosome replication in the seqA strain was not reversed in the mukBseqA double mutant [10].
• Introduction of the wild-type seqA gene on a low-copy plasmid suppresses the cold sensitivity of a dnaAcos mutant known to overinitiate at temperatures below 39 degrees C. In addition, the seqA2 mutation is a suppressor of several dnaA (Ts) alleles [11].

Anatomical context of seqA

• We present evidence that biological properties of cell membranes are altered in dnaA and seqA mutants of Escherichia coli relative to wild-type bacteria [12].

Associations of seqA with chemical compounds

• The dam mutant showed an accumulation of the acidic phospholipids cardiolipin, whereas, the seqA mutant showed a higher proportion of phosphatidylglycerol compared with the wild-type strain [13].

Other interactions of seqA

• Site specific binding to hemimethylated oriC, of the heavy density membrane obtained from seqA mutant, could be restored by addition of a low amount of His-tagged SeqA protein [14].

Analytical, diagnostic and therapeutic context of seqA

• Flow cytometry demonstrated that the fusion restored synchronous replication of chromosomal DNA from multiple origins in seqA null mutant cells, indicating that SeqA-Gfp is biologically active [15].
• A possible reason for this failure might be a profound modification of the outer membrane of the seqA mutant (as revealed by the fact that membrane from the mutant sediments more slowly than that from the wild type during ultracentrifugation) [16].

References