Abstract
Using tiling microarrays, a mechanism by which Plasmodium falciparum parasites acquire resistance to the antimalarial fosmidomycin has been elucidated
Highlights
The identification of genetic changes that confer drug resistance or other phenotypic changes in pathogens can help optimize treatment strategies, support the development of new therapeutic agents, and provide information about the likely function of genes
Identifying the genetic changes that are involved in drug resistance or other phenotypic changes can help with the development of effective therapies, improve understanding of parasite biology and gene function, and assist in elucidating the mode of action of uncharacterized chemical compounds that exhibit antimalarial activity in high-throughput cellular screening campaigns [5,6,7]
Each nucleotide in the coding genome could be probed from 9 to 13 times on the microarray. This probe density allows for detection of polymorphisms within a distance of several nucleotides, and the density is much greater than our previous P. falciparum microarray that had 327,989 non-overlapping 25 mer oligonucleotide probes spaced approximately every 50 base pairs [22] or the microarray, used for single nucleotide polymorphism (SNP) and copy number variation (CNV) detection, designed at The Sanger Institute that has about 2.5 million probes [26]
Summary
The identification of genetic changes that confer drug resistance or other phenotypic changes in pathogens can help optimize treatment strategies, support the development of new therapeutic agents, and provide information about the likely function of genes. With many complete eukaryotic genomes and draft eukaryotic sequencing projects deposited in the National Center for Biotechnology Information database, attention is shifting to discovering genomic diversity and associating this genetic variation with defined phenotypes This is of particular interest with the human malarial parasite Plasmodium falciparum, whose extensive genetic variability and sexual recombination facilitates the emergence and spread of drug resistance [1,2], resulting in treatment failure for many of the licensed antimalarial agents [3,4]. Identifying the genetic changes that are involved in drug resistance or other phenotypic changes can help with the development of effective therapies, improve understanding of parasite biology and gene function, and assist in elucidating the mode of action of uncharacterized chemical compounds that exhibit antimalarial activity in high-throughput cellular screening campaigns [5,6,7]. The median for each bin was set to the median of the corresponding bin in the synthetic baseline microarray
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