PL EN


Preferences help
enabled [disable] Abstract
Number of results
Journal
2002 | 51 | 3 | 305-318
Article title

Partycja niskokopiowych plazmidów

Content
Title variants
EN
Partitioning of low-copy number plasmids
Languages of publication
PL EN
Abstracts
EN
Summary Partitioning of low-copy number plasmids at cell division resembles mitosis in that prior to cell division paired plasmid molecules are separated from each other and actively moved apart from the center of the mother cell into positions corresponding to the centers of future daughters. Two plasmid proteins and a cis-acting site in plasmid DNA, an analog of eukaryotic centromere, are essential for partitioning to occur. Typically, partition proteins are encoded within an operon whose expression is regulated by one or both of its products. The product of the first gene of the partition operon (ParA, SopA or ParM) is an ATPase, the product of the second gene (ParB, SopB or ParR) is a centromere-binding protein. Partitioning ATPases belong to the Walker-type or actin-type ATPase families. They interact with their target centromeric complexes indirectly, via plasmid specific centromere- binding proteins. Two types of partitioning ATPases may provide two different ways of plasmid translocation within a cell. The movement of plasmid Rl, which encodes the actin-type ParM ATPase, is associated with extension of ParM filaments at their polar end and depolymerization at the opposite end. Extension might possibly occur by insertion of new ParM molecules between the centromere-bound ParR proteins of paired Rl plasmids and ParM molecules bound to ParR, thus pushing the plasmids towards the opposite cell poles. The role of Walker-type ATPases in plasmid translocation is not clear. In their structure they resemble some ion pump proteins. They may either participate in plasmid movement by themselves or connect plasmids to unknown partition machinery of a host. Some of them can oscillate between cellular poles, reminiscent of the behavior of related bacterial proteins, MinD, that specify the sites of septum placement. Partitioning mechanisms in bacteria are evolutionarily conserved and of universal occurrence. Plasmid partition operons with centromeric sites can function as gene cassettes able to stabilize other unstable low-copy number plasmids. Certain bacterial chromosomes encode homologs of plasmid partition genes essential for chromosome partitioning.
Keywords
Journal
Year
Volume
51
Issue
3
Pages
305-318
Physical description
Dates
published
2002
Contributors
  • Zakład Biochemii Drobnoustrojów Instytut Biochemii i Biofizyki PAN, Pawińskiego 5A, 02-106 Warszawa, Polska
author
  • Zakład Biochemii Drobnoustrojów Instytut Biochemii i Biofizyki PAN, Pawińskiego 5A, 02-106 Warszawa, Polska
author
  • Zakład Biochemii Drobnoustrojów Instytut Biochemii i Biofizyki PAN, Pawińskiego 5A, 02-106 Warszawa, Polska
References
  • ABELES, A. L., FRIEDMAN S. A., AUSTIN S. J., 1985. Partition of unit-copy miniplasmids to daughter cells. III. The DNA sequence and functional organization of the P1 partition region. J. Mol. Biol. 185, 261-272.
  • AUSTIN S., FRIEDMAN S., LUDTKE D., 1986. Partition functions of unit-copy plasmids can stabilize the maintenance of plasmid pBR322 at low copy number. J. Bacteriol. 168, 1010-103.
  • AUSTIN S., NORDSTROM K., 1990. Partition-mediated incompatibility of bacterial plasmids. Cell 60, 351-354.
  • AUSTIN S. J., 1984. Bacterial plasmids that carry two functional centromere analogs are stable and are partitioned faithfully. J. Bacteriol. 158, 742-745.
  • BARTOSIK D., 2001. Bacterial plasmid stability. Postepy Biochem. 47, 138-145.
  • BARTOSIK D., BAJ J., PIECHUCKA E., WALKER E., WŁODARCZYK M., 2002. Comparative characterization of repABC-type replicons of Paracoccus versutus composite plasmids. Plasmid (w druku).
  • BIEK D. P., SHI J., 1994. A single 43-bp sopC repeat of plasmid mini-F is sufficient to allow assembly of a functional nucleoprotein partition complex. Proc. Natl. Acad. Sci. USA 91, 8027-8031.
  • BIGNELL C., THOMAS C. M., 2001 The bacterial ParA-ParB partitioning proteins. J. Biotechnol. 91, 1-34.
  • BIGNELL C. R., HAINES A. S., KHARE D., THOMAS, C. M., 1999. Effect of growth rate and incC mutation on symmetric plasmid distribution by the IncP-1 partitioning apparatus. Mol. Microbiol. 34, 205-216.
  • BORK P., SANDER C., VALENCIA A., 1992. An ATPase domain common to prokaryotic cell cycle proteins, sugar kinases, actin, and hsp70 heat shock proteins. Proc. Natl. Acad. Sci. USA 89, 7290-7294.
  • BOUET J. Y., FUNNELL B. E., 1999. P1 ParA interacts with the P1 partition complex at parS and an ATP-ADP switch controls ParA activities. Embo J. 18, 1415-1424.
  • BREUNER A., JENSEN R. B., DAM M., PEDERSEN S., GERDES K., 1996. The centromere-like parC locus of plasmid R1. Mol. Microbiol. 20, 581-592.
  • DAM M., GERDES K., 1994. Partitioning of plasmid R1. Ten direct repeats flanking the parA promoter constitute a centromere-like partition site parC, that expresses incompatibility. J Mol. Biol. 236, 1289-1298.
  • DAVEY M. J., FUNNELL B. E., 1994. The P1 plasmid partition protein ParA. A role for ATP in site-specific DNA binding. J. Biol. Chem. 269, 29908-29913.
  • DAVEY M. J., FUNNELL B. E., 1997. Modulation of the P1 plasmid partition protein ParA by ATP, ADP, and P1 ParB. J. Biol. Chem. 272, 15286-15292.
  • DAVIS M. A., MARTIN K. A., AUSTIN S. J., 1992. Biochemical activities of the parA partition protein of the P1 plasmid. Mol. Microbiol. 6, 1141-1147.
  • DAVIS M. A., RADNEDGE L., MARTIN K. A., HAYES F., YOUNGREN B., AUSTIN S. J., 1996. The P1 ParA protein and its ATPase activity play a direct role in the segregation of plasmid copies to daughter cells. Mol. Microbiol. 21, 1029-1036.
  • DE LA HOZ A. B., AYORA S., SITKIEWICZ I., FERNANDEZ S., PANKIEWICZ R., ALONSO J.C., CEGŁOWSKI P., 2000. Plasmid copy-number control and better-thanrandom segregation genes of pSM19035 share a common regulator. Proc. Natl. Acad. Sci. USA 97, 728-733.
  • EBERSBACH G., GERDES, K., 2001. The double par locus of virulence factor pB171: DNA segregation is correlated with oscillation of ParA. Proc. Natl. Acad. Sci. USA 98, 15078-15083.
  • EDGAR R., CHATTORAJ D. K., YARMOLINSKY M., 2001. Pairing of P1 plasmid partition sites by ParB. Mol. Microbiol. 42, 1363-70.
  • ERDMANN N., PETROFF T., FUNNELL B.E., 1999. Intracellular localization of P1 ParB protein depends on ParA and parS. Proc. Natl. Acad. Sci. USA 96, 14905-14910.
  • FUNG E., BOUET J.Y., FUNNELL B. E., 2001. Probing the ATP-binding site of P1 ParA: partition and repression have different requirements for ATP binding and hydrolysis. EMBO J. 20, 4901-4911.
  • FUNNELL B. E., 1988a. Mini-P1 plasmid partitioning: excess ParB protein destabilizes plasmids containing the centromere parS. J. Bacteriol. 170, 954-960.
  • FUNNELL B. E., 1988b. Participation of Escherichia coli integration host factor in the P1 plasmid partition system. Proc. Natl. Acad. Sci. USA 85, 6657-6661.
  • FUNNELL B. E., 1991. The P1 plasmid partition complex at parS. The influence of Escherichia coli integration host factor and of substrate topology. J. Biol. Chem. 266, 14328-14337.
  • FUNNELL B. E., GAGNIER L., 1993. The P1 plasmid partition complex at parS. II. Analysis of ParB protein binding activity and specificity. J. Biol. Chem. 268, 3616-3624.
  • GERDES K., MOLLER-JENSEN J., BUGGE JENSEN R., 2000. Plasmid and chromosome partitioning: surprises from phylogeny. Mol. Microbiol. 37, 455-466.
  • GODFRIN-ESTEVENON A. M., PASTA F., LANE D., 2002. The parAB gene products of Pseudomonas putida exhibit partition activity in both P. putida and Escherichia coli. Mol. Microbiol. 43, 39-49.
  • GORDON G. S., SITNIKOV D., WEBB C. D., TELEMAN A., STRAIGHT A., LOSICK R., MURRAY A. W., WRIGHT A., 1997. Chromosome and low copy plasmid segregation in E. coli: visual evidence for distinct mechanisms. Cell 90, 1113-1121.
  • GRIGORIEV P., ŁOBOCKA M. B., 2001. Determinants of segregational stability of the linear plasmid prophage N15 of Escherichia coli. Mol. Microbiol. 42, 355-368..
  • HANAI R., LIU R., BENEDETTI P., CARON P. R., LYNCH A. S., WANG J. C., 1996. Molecular dissection of a protein SopB essential for Escherichia coli F plasmid partition. J. Biol. Chem. 271, 17469-17475.
  • HAO J. J., YARMOLINSKY M., 2002. Effects of the plasmid centromere on expression of P1 partition genes. J. Bacteriol. 184, 4857-4867.
  • HAYES F., AUSTIN S., 1994. Topological scanning of the P1 plasmid partition site. J. Mol. Biol. 243, 190-198.
  • HIRAGA S., 2000. Dynamic localization of bacterial and plasmid chromosomes. Annu. Rev. Genet. 34, 21-59.
  • HIRANO M., MORI H., ONOGI T., YAMAZOE M., NIKI H., OGURA T., HIRAGA S., 1998. Autoregulation of the partition genes of the mini-F plasmid and the intracellular localization of their products in Escherichia coli. Mol. Gen. Genet. 257, 392-403.
  • HO T. Q., ZHONG Z., AUNG S., POGLIANO J., 2002. Compatible bacterial plasmids are targeted to independent cellular locations in Escherichia coli. EMBO J. 21, 1864-1872.
  • JAGURA-BURDZY G., MACARTNEY D. P., ZATYKA M., CUNLIFFE L., COOKE D., HUGGINS C., WESTBLADE L., KHANIM F., THOMAS C. M., 1999. Repression at a distance by the global regulator KorB of promiscuous IncP plasmids. Mol. Microbiol. 32, 519-532.
  • JENSEN R. B., DAM M., GERDES K., 1994. Partitioning of plasmid R1. The parA operon is autoregulated by ParR and its transcription is highly stimulated by a downstream activating element. J. Mol. Biol. 236, 1299-1309.
  • JENSEN R. B., GERDES K., 1997. Partitioning of plasmid R1. The ParM protein exhibits ATPase activity and interacts with the centromere-like ParR-parC complex. J. Mol. Biol. 269, 505-513.
  • JENSEN R. B., GERDES K., 1999. Mechanism of DNA segregation in prokaryotes: ParM partitioning protein of plasmid R1 co-localizes with its replicon during the cell cycle. EMBO J. 18, 4076-4084.
  • JENSEN R. B., LURZ R., GERDES K., 1998. Mechanism of DNA segregation in prokaryotes: replicon pairing by parC of plasmid R1. Proc. Natl. Acad. Sci. USA 95, 8550-8555.
  • JONES L. J., CARBALLIDO-LOPEZ R., ERRINGTON J., 2001. Control of cell shape in bacteria: helical, actin-like filaments in Bacillus subtilis. Cell 104, 913-922.
  • KALNIN K., STEGALKINA S., YARMOLINSKY M., 2000. pTAR-encoded proteins in plasmid partitioning. J. Bacteriol. 182, 1889-1894.
  • KIM S. K., WANG J. C., 1999. Gene silencing via protein-mediated subcellular localization of DNA. Proc. Natl. Acad. Sci. USA 96, 8557-8561.
  • KOONIN E. V., 1993. A superfamily of ATPases with diverse functions containing either classical or deviant ATP-binding motif [published erratum appears in J. Mol. Biol. 1993232(3), 1013]. J. Mol. Biol. 229, 1165-1174.
  • KUSUKAWA N., MORI H., KONDO A., HIRAGA S., 1987. Partitioning of the F plasmid: overproduction of an essential protein for partition inhibits plasmid maintenance. Mol. Gen. Genet. 208, 365-372.
  • LANE D., ROTHENBUEHLER R., MERRILLAT A. M., AIKEN C. 1987. Analysis of the F plasmid centromere. Mol. Gen. Genet. 207, 406-412.
  • LEMON K. P., GROSSMAN A. D., 1998. Localization of bacterial DNA polymerase: evidence for a factory model of replication [see comments]. Science 282, 1516-159.
  • LEMON K. P., GROSSMAN A. D., 2000. Movement of replicating DNA through a stationary replisome. Mol. Cell 6, 1321-1330.
  • LIN D. C., GROSSMAN A. D., 1998. Identification and characterization of a bacterial chromosome partitioning site. Cell 92, 675-685.
  • LOBOCKA M., YARMOLINSKY M., 1996. P1 plasmid partition: a mutational analysis of ParB. J. Mol. Biol. 259, 366-382.
  • MARTIN K. A., DAVIS M. A., AUSTIN S., 1991. Fine-structure analysis of the P1 plasmid partition site. J. Bacteriol. 173, 3630-3634.
  • MOHL D. A., GOBER J. W., 1997. Cell cycle-dependent polar localization of chromosome partitioning proteins in Caulobacter crescentus. Cell 88, 675-684.
  • MOLLER-JENSEN J., JENSEN R. B., LOWE J., GERDES K., 2002. Prokaryotic DNA segregation by an actin-like filament. EMBO J. 21, 3119-3127.
  • MORI H., MORI Y., ICHINOSE C., NIKI H., OGURA T., KATO A., HIRAGA S., 1989. Purification and characterization of SopA and SopB proteins essential for F plasmid partitioning. J. Biol. Chem. 264, 15535-15541.
  • POGLIANO J., HO T. Q., ZHONG Z., HELINSKI D. R., 2001. Multicopy plasmids are clustered and localized in Escherichia coli. Proc. Natl. Acad. Sci. USA 98, 4486-4491.
  • QUISEL J. D., LIN D. C., GROSSMAN A. D., 1999. Control of development by altered localization of a transcription factor in B. subtilis. Mol. Cell 4, 665-672.
  • RASKIN D. M., DE BOER P. A.,1999. Rapid pole-to-pole oscillation of a protein required for directing division to the middle of Escherichia coli. Proc. Natl. Acad. Sci. USA 96, 4971-4976.
  • RAVIN N., LANE D., 1999. Partition of the linear plasmid N15: interactions of N15 partition functions with the sop locus of the F plasmid. J. Bacteriol. 181, 6898-6906.
  • RODIONOV O., LOBOCKA M., YARMOLINSKY M., 1999. Silencing of genes flanking the P1 plasmid centromere. Science 283, 546-549.
  • STRZELECKA-GOLASZEWSKA H., 2001. Generacja ruchu przez polimeryzację aktyny. Kosmos, 50, 411-425.
  • TREPTOW N., ROSENFELD R., YARMOLINSKY M., 1994 Partition of nonreplicating DNA by the par system of bacteriophage P1. J. Bacteriol. 176, 1782-1786.
  • VAN DEN ENT F., AMOS L. A., LOWE J., 2001. Prokaryotic origin of the actin cytoskeleton. Nature 413, 39-44.
  • WEITAO T., DASGUPTA S., NORDSTROM K., 2000. Plasmid R1 is present as clusters in the cells of Escherichia coli. Plasmid 43, 200-204.
  • YAMAICHI Y., NIKI H., 2000. Active segregation by the bacillus subtilis partitioning system in Escherichia coli. Proc. Natl. Acad. Sci. USA 97, 14656-14661.
  • YARMOLINSKY M., 2000. Transcriptional silencing in bacteria. Curr. Opin. Microbiol. 3, 138-143.
Document Type
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.bwnjournal-article-ksv51p305kz
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.