Inhibition of in vitro splicing of a group I intron of Pneumocystis carinii.
Unlike its mammalian hosts, the opportunistic fungal pathogen Pneumocystis carinii harbors group I self-splicing introns in its chromosomal genes encoding rRNA. This difference between pathogen and host suggests that intron splicing is a promising target for chemotherapy. We have found that intron splicing in vitro is inhibited by the anti-Pneumocystis agent pentamidine and by a series of pentamidine analogues, as well as by some aminoglycosides, tetracycline, L-arginine and ethidium bromide. Further studies will be needed to determine if this is the mechanism of action of pentamidine against P. carinii.
Liu
Y
Y
Department of Molecular Genetics, and Microbiology, UMDNJ-Robert Wood Johnson Medical School, Piscataway 08854-5635.
Tidwell
R R
RR
Leibowitz
M J
MJ
D001483:Base Sequence; D017931:DNA Primers; D006160:Guanosine Triphosphate / Q000378:metabolism; D007438:Introns; D007700:Kinetics; D008969:Molecular Sequence Data; D010419:Pentamidine / Q000031:analogs & derivatives / Q000494:pharmacology*; D011010:Pneumocystis / Q000187:drug effects* / Q000235:genetics; D012326:RNA Splicing / Q000187:drug effects*; D012331:RNA, Fungal / Q000187:drug effects / Q000235:genetics
D017931:DNA Primers; D012331:RNA, Fungal; D010419:Pentamidine; D006160:Guanosine Triphosphate