SeqA: A negative modulator of replication initiation in E. coli

Lü, Min; Campbell, Joseph L.; Boye, Erik; Kleckner, Nancy

doi:10.1016/0092-8674(94)90156-2

Cited by 479 publications

(715 citation statements)

References 55 publications

Supporting

Mentioning

671

Contrasting

Unclassified

Order By: Relevance

“…The dam-13::Tn9 mutation inhibits growth of the temperature-sensitive dnaA46 mutant at a semi-permissive temperature of 37ЊC (Lu et al, 1994). We found that the growth of NA156 [dnaA46 aroK::Tn5 ] and NA157 [dnaA46 aroB::Tn5 ] was completely inhibited at 37ЊC; at 35ЊC or below, the double mutants grew (data not shown).…”

Section: Cellular Dnaa Concentration In Suppressed Strainsmentioning

confidence: 73%

“…Factors such as nucleoid proteins (Kano et al, 1991;Filutowicz et al, 1992;Katayama et al, 1996b), transcription around oriC (Asai et al, 1990;Theisen et al, 1993;Ogawa and Okazaki, 1994) and titration of DnaA protein on a chromosome site of 94.7 min (Kitagawa et al, 1996) participate in initiation control. SeqA protein prevents extra reinitiation (Lu et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Overinitiation of chromosome replication in the Escherichia coli dnaAcos mutant depends on activation of oriC function by the dam gene product

Katayama

Akimitsu

Mizushima

et al. 1997

Molecular Microbiology

View full text Add to dashboard Cite

show abstract

Section: Cellular Dnaa Concentration In Suppressed Strainsmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Overinitiation of chromosome replication in the Escherichia coli dnaAcos mutant depends on activation of oriC function by the dam gene product

Katayama

Akimitsu

Mizushima

et al. 1997

Molecular Microbiology

View full text Add to dashboard Cite

show abstract

“…Dam methylation also helps to regulate chromosome replication by maintaining the methylation of the origin of chromosome replication. For example, DNA replication is controlled in part by the SeqA protein, which binds specifically to hemimethylated GATC sites near the origin of replication and delays their full methylation [14][15][16] . Dam methylation regulates the expression of certain genes in E. coli 17,18 , the yopE gene in Yersinia pseudotuberculosis 19 , and phage Mu mom gene (reviewed in ref.…”

mentioning

confidence: 99%

Structure of the bacteriophage T4 DNA adenine methyltransferase

Yang

Horton

Zhou

et al. 2003

Nat Struct Mol Biol

View full text Add to dashboard Cite

DNA-adenine methylation at certain GATC sites plays a pivotal role in bacterial and phage gene expression as well as bacterial virulence. We report here the crystal structures of the bacteriophage T4Dam DNA adenine methyltransferase (MTase) in a binary complex with the methyl-donor product S-adenosyl-L-homocysteine (AdoHcy) and in a ternary complex with a synthetic 12-bp DNA duplex and AdoHcy. T4Dam contains two domains: a seven-stranded catalytic domain that harbors the binding site for AdoHcy and a DNA binding domain consisting of a five-helix bundle and a β-hairpin that is conserved in the family of GATC-related MTase orthologs. Unexpectedly, the sequence-specific T4Dam bound to DNA in a nonspecific mode that contained two Dam monomers per synthetic duplex, even though the DNA contains a single GATC site. The ternary structure provides a rare snapshot of an enzyme poised for linear diffusion along the DNA.DNA MTases catalyze methyl group transfer from donor S-adenosyl-L-methionine (AdoMet), producing S-adenosyl-L-homocysteine (AdoHcy) and methylated DNA. Although most prokaryote DNA MTases are components of restriction-modification systems, some MTases are not associated with cognate restriction enzymes, such as the Escherichia coli DNA adenine MTase (Dam). This enzyme methylates an exocyclic amino nitrogen (N6) of the adenine in GATC 1,2 . Dam MTase gene orthologs are widespread among enteric bacteria and their bacteriophages (see Fig. 1 legend). Dam methylation is not essential for the viability of E. coli, unless it is combined with certain other mutations 3 ; however, Dam is an essential gene in Vibrio cholerae and Yersinia pesudotuberculosis, at least under the tested growth conditions 4 . Dam methylation is essential for the virulence of Salmonella serovar typhimurium in a murine model of typhoid fever [5][6][7] . These observations COMPETING INTERESTS STATEMENTThe authors declare that they have no competing financial interests. NIH Public Access RESULTS Overall structure of DamThe monomeric Dam structure contains 9 β-strands and 11 α-helices (Fig. 1). The Nterminal region (residues 1-52) and C-terminal region (residues 149-259) come together, forming the catalytic domain (green in Figs. 1 and 2a) with a seven-stranded β-sheet, a characteristic feature of the class-I AdoMet-dependent MTases 28 . The N-terminal helices αZ and αA are located on one side of the β-sheet, and helices αC, αD1 and αD2 and αE are on the other side. Between strands β2 and β3 is a separate domain, which we designate as the target-recognition domain (TRD). TRD is composed of a five-helix bundle (αB1-αB5) (yellow in Figs. 1 and 2a) and a 25-residue segment containing a β-hairpin (β8 and β9) inserted between helices αB4 and αB5 (red). The overall dimensions of the molecule are 55 × 34 × 28 Å, with an open cleft located between the catalytic domain (green) and the TRD (yellow and red). Conserved residues and the effects of mutationsBased on the linear arrangement of conserved motifs in DNA MTases, T4Dam is classified in the...

show abstract

“…The density-shift analysis was performed in a seqA+ strain. However, the time after initiation when oriC is sequestered and unavailable for reinitiation is approximately 6-8 min at 30°C (Lu et a/., 1994;Ogden et a/., 1988), while the eclipse period measured in our density-shift analysis was substantially longer (more than 30min; Fig. 2).…”

Section: Discussionmentioning

confidence: 65%

“…One cause for such a delay is sequestration of oriC by the SeqA protein (Lu et a/., 1994). The density-shift analysis was performed in a seqA+ strain.…”

Section: Discussionmentioning

confidence: 99%

Replication of minichromosomes in a host in which chromosome replication is random

Eliasson

Nordström

1997

Molecular Microbiology

View full text Add to dashboard Cite

SummaryMinichromosomes are plasmids with the origin of chromosome replication, oriC, as their only origin of replication. In Escherichia coli, minichromosomes are compatible with the chromosome and replicate in a cell-cycle-specific manner at the same time as oriC located on the chromosome initiates replication. In int strains, oriC has been inactivated and replaced by a plasmid origin. Because plasmids control their own replication, chromosome replication is uncoupled from the normal cell-cycle control and is random with respect to the cell cycle in the int strains. We have used an intP7 strain to address thequestion of whether minicromosome replication i s coupled to the replication of the chromosome or is governed by cellcycle-specific signals. Minichromosome replication was analysed by density-shift experiments and found not to be random in the randomly replicating intP7 host. This suggests that the cell-cycle-specific control functions of oriC replication are operating also in the intP7 strain.

show abstract

SeqA: A negative modulator of replication initiation in E. coli

Cited by 479 publications

References 55 publications

Overinitiation of chromosome replication in the Escherichia coli dnaAcos mutant depends on activation of oriC function by the dam gene product

Overinitiation of chromosome replication in the Escherichia coli dnaAcos mutant depends on activation of oriC function by the dam gene product

Structure of the bacteriophage T4 DNA adenine methyltransferase

Replication of minichromosomes in a host in which chromosome replication is random

Contact Info

Product

Resources

About