Positional cloning of a sequence from the breakpoint of chromosome 9 commonly associated with the loss of cytoadherence.
Isolates of Plasmodium falciparum commonly undergo a large, subtelomeric deletion of the right end of chromosome 9 during in-vitro cultivation. This deletion is usually accompanied by loss of ability to cytoadhere to melanoma cells, loss of a var-gene product from the red-cell surface and a reduction in gametocyte production. However, cytoadherence is stable in the isolate ItG2, remaining after many generations in culture. Deletions in all the non-cytoadherent clones examined have breakpoints within or delete a novel open-reading frame, called the breakpoint open-reading frame (BPORF), that is a unique sequence in the genome. In ItG2, surprisingly, BPORF has been removed by a 15-kb deletion, internal in chromosome 9. These results indicate mechanisms to explain why the deletion of chromosome 9 occurs so frequently and why cytoadherence is stable in ItG2.
Bourke
P F
PF
Menzies School of Health Research, Casuarina, Australia.
Holt
D C
DC
Sutherland
C J
CJ
Currie
B
B
Kemp
D J
DJ
D000818:Animals; D002448:Cell Adhesion / Q000235:genetics*; D002869:Chromosome Aberrations; D002874:Chromosome Mapping; D002899:Chromosomes, Human, Pair 9; D006801:Humans; D010963:Plasmodium falciparum / Q000235:genetics*