Linked Life Data

3056622

Source:http://linkedlifedata.com/resource/pubmed/id/3056622

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1989-1-4
pubmed:databankReference
pubmed:abstractText
The human malaria parasite P. falciparum exhibits extensive strain-dependent chromosomal polymorphisms that have been implicated in the generation of antigenic variability in this organism. These polymorphisms can result in large deletions in chromosomes as determined by pulsed-field gradient gel electrophoresis. We have investigated the molecular basis for extensive deletions in chromosomes 2 and 8 in multiple geographic isolates of this parasite that result in the loss of expression of well-characterized parasite antigens. The structure of these polymorphic chromosomes reveal that a mechanism of chromosome breakage and healing by the addition of telomeric repeats most plausibly accounts for these karyotypes. Furthermore, the orientation of these gene fragments on their truncated chromosomes reveal that the healed chromosome originally associated with centromeric elements is mitotically stable and maintained. A model for the possible role of this mechanism in the complex parasite life-cycle is discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
55
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
869-74
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
Large deletions result from breakage and healing of P. falciparum chromosomes.
pubmed:affiliation
DeWitt Wallace Research Laboratory, Sloan-Kettering Institute, New York, New York 10021.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't