Linked Life Data

10931340

Source:http://linkedlifedata.com/resource/pubmed/id/10931340

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-9-12
pubmed:abstractText
Replication origins of a family of bacterial plasmids have multiple sites, called iterons, for binding a plasmid-specific replication initiator protein. The iteron-initiator interactions are essential for plasmid replication as well as for inhibition of plasmid over-replication. The inhibition increases with plasmid copy number and eventually shuts plasmid replication off completely. The mechanism of inhibition appears to be handcuffing, the coupling of origins via iteron-bound initiators that block origin function. The probability of a trans-reaction such as handcuffing is expected to increase with plasmid copy number and diminish with increases in cell volume, explaining how the copy number can be maintained in a growing cell. Control is also exerted at the level of initiator synthesis and activation by chaperones. We propose that increases in active initiators promote initiation by overcoming handcuffing, but handcuffing dominates when the copy number reaches a threshold. Handcuffing should be ultrasensitive to copy number, as the negative control by iterons can be stringent (switch-like).
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
37
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
467-76
pubmed:dateRevised
2006-5-1
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Control of plasmid DNA replication by iterons: no longer paradoxical.
pubmed:affiliation
Laboratory of Biochemistry, NCI, NIH, Bethesda, MD 20892-4255, USA. dhrubac@sunspot.nci.nih.gov
pubmed:publicationType
Journal Article, Review