RT Journal
A1 Miles, Alistair
A1 Iqbal, Zamin
A1 Vauterin, Paul
A1 Pearson, Richard
A1 Campino, Susana
A1 Theron, Michel
A1 Gould, Kelda
A1 Mead, Daniel
A1 Drury, Eleanor
A1 O'Brien, John
A1 Ruano Rubio, Valentin
A1 MacInnis, Bronwyn
A1 Mwangi, Jonathan
A1 Samarakoon, Upeka
A1 Ranford-Cartwright, Lisa
A1 Ferdig, Michael
A1 Hayton, Karen
A1 Su, Xin-zhuan
A1 Wellems, Thomas
A1 Rayner, Julian
A1 McVean, Gil
A1 Kwiatkowski, Dominic
T1 Indels, structural variation, and recombination drive genomic diversity in Plasmodium falciparum
JF Genome Research 
JO Genome Research 
YR 2016 
FD September 01 
VO 26 
IS 9 
SP 1288 
OP 1299 
DO 10.1101/gr.203711.115 
UL http://genome.cshlp.org/content/26/9/1288.abstract 
AB The malaria parasite Plasmodium falciparum has a great capacity for evolutionary adaptation to evade host immunity and develop drug resistance. Current understanding of parasite evolution is impeded by the fact that a large fraction of the genome is either highly repetitive or highly variable and thus difficult to analyze using short-read sequencing technologies. Here, we describe a resource of deep sequencing data on parents and progeny from genetic crosses, which has enabled us to perform the first genome-wide, integrated analysis of SNP, indel and complex polymorphisms, using Mendelian error rates as an indicator of genotypic accuracy. These data reveal that indels are exceptionally abundant, being more common than SNPs and thus the dominant mode of polymorphism within the core genome. We use the high density of SNP and indel markers to analyze patterns of meiotic recombination, confirming a high rate of crossover events and providing the first estimates for the rate of non-crossover events and the length of conversion tracts. We observe several instances of meiotic recombination within copy number variants associated with drug resistance, demonstrating a mechanism whereby fitness costs associated with resistance mutations could be compensated and greater phenotypic plasticity could be acquired.