Chromosomal rearrangements and point mutations in the DHFR-TS gene of Plasmodium chabaudi under antifolate selection
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On the contribution of the rodent model Plasmodium chabaudi for understanding the genetics of drug resistance in malaria
2022, Parasitology InternationalCitation Excerpt :SDX resistance in P. falciparum has been linked with several point mutations on the pppk-dhps gene: S436A, A437G, K540E, A581G and A613S,T [40,41,42]. In the experimentally evolved P. chabaudi AS-PYR clone (Fig. 1) a DHFR S106N [21,43,44] mutation was selected (Fig. 3), which is homologous to S108N in P. falciparum. Interestingly, as also reported in P. falciparum [45], the acquisition of PYR resistance in P. chabaudi is accompanied by an increase in susceptibility to SDX [46].
Whole genome re-sequencing identifies a mutation in an ABC transporter (mdr2) in a Plasmodium chabaudi clone with altered susceptibility to antifolate drugs
2011, International Journal for ParasitologyCitation Excerpt :Those four mutations were confirmed by amplification and di-deoxy sequencing, and their origin within the AS lineage determined by sequencing AS-sens, AS-PYR1 and AS-50S/P (Fig. 1). DHFR S106N has previously been characterised (Cowman and Lew, 1990; Cheng and Saul, 1994) and arises, as expected, in AS-PYR1 during PYR selection. The intergenic point mutation on chr14 (T936,945G) was confirmed by dideoxy sequencing as appearing first in AS-PYR1.
Chloroquine resistance in Plasmodium chabaudi: Are chloroquine-resistance transporter (crt) and multi-drug resistance (mdr1) orthologues involved?
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2001, Trends in ParasitologyA method for the sequential study of eimerian chromosomes by light and electron microscopy
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