A and T homopolymeric stretches mediate a DNA inversion in Plasmodium falciparum which results in loss of gene expression.
Ring-infected erythrocyte surface antigen-negative isolates of Plasmodium falciparum demonstrate a complex DNA rearrangement with inversion of 5' coding sequences, deletion of upstream and flanking sequences, and healing of the truncated chromosome by telomere addition. An inversion intermediate that results in the telomeric gene structure for RESA has been identified in the pathway. This inversion creates a mitotically stable substrate for the sequence-specific addition of telomere repeats at the deletion breakpoint.
Pologe
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LG
Sloan-Kettering Institute, New York, New York 10021.
de Bruin
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D
Ravetch
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JV
D000818:Animals; D000953:Antigens, Protozoan / Q000235:genetics; D000954:Antigens, Surface / Q000235:genetics*; D001483:Base Sequence; D015139:Blotting, Southern; D002872:Chromosome Deletion; D007446:Chromosome Inversion; D002874:Chromosome Mapping; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D008969:Molecular Sequence Data; D015345:Oligonucleotide Probes; D010963:Plasmodium falciparum / Q000235:genetics*; D016133:Polymerase Chain Reaction; D015800:Protozoan Proteins; D015183:Restriction Mapping
D000953:Antigens, Protozoan; D000954:Antigens, Surface; D015345:Oligonucleotide Probes; D015800:Protozoan Proteins; C050256:ring-infected erythrocyte surface antigen (RESA), Plasmodium falciparum; D004247:DNA