Divergence With Gene Flow in Anopheles funestus From the Sudan Savanna of Burkina Faso, West Africa

Abstract

Anopheles funestus is a major vector of malaria across Africa. Understanding its complex and nonequilibrium population genetic structure is an important challenge that must be overcome before vector populations can be successfully perturbed for malaria control. Here we examine the role of chromosomal inversions in structuring genetic variation and facilitating divergence in Burkina Faso, West Africa, where two incipient species (chromosomal forms) of A. funestus, defined principally by rearrangements of chromosome 3R, have been hypothesized. Sampling across an $300-km east-west transect largely contained within the Sudan-Savanna ecoclimatic zone, we analyzed chromosomal inversions, 16 microsatellite loci distributed genomewide, and 834 bp of the mtDNA ND5 gene. Both molecular markers revealed high genetic diversity, nearly all of which was accounted for by within-population differences among individuals, owing to recent population expansion. Across the study area there was no correlation between genetic and geographic distance. Significant genetic differentiation found between chromosomal forms on the basis of microsatellites was not genomewide but could be explained by chromosome 3R alone on the basis of loci inside and near inversions. These data are not compatible with complete reproductive isolation but are consistent with differential introgression and sympatric divergence between the chromosomal forms, facilitated by chromosome 3R inversions.

Effective population size of Anopheles funestus chromosomal forms in Burkina Faso

“…All loci were found to be in linkage equilibrium. Significant Hardy-Weinberg deficits occurred in 12 of 96 possible tests, but were clustered at 3 loci (AFND12, FunD, and AFUB12) suspected of harboring null alleles [6,7]. …”

“…Mitochondrial sequences (834 bp of the ND5 gene) were taken from Michel et al [6], based on 90 Folonzo and 96 Kiribina samples collected from La and Pehele, Burkina Faso in 2002 [GenBank, Kiribina: DQ126772–DQ126867; Folonzo: DQ127048–DQ127137]. There was no significant mtDNA or microsatellite differentiation between these locales for samples of the same chromosomal form [6].…”

“…There was no significant mtDNA or microsatellite differentiation between these locales for samples of the same chromosomal form [6]. …”

“…The relative abundance of Kiribina near rice cultivation and Folonzo near marshy areas suggests some partitioning of larval habitats, and the latter form is more likely to rest indoors, feed on humans, and be infected with malaria parasites [4]. At the molecular level, differentiation between forms is slight and is accounted for mainly by markers mapping to the chromosome arm (3R) bearing the principal inversions whose frequencies define the forms [6,7]. The working hypothesis is that Folonzo and Kiribina forms of An.…”

Variation in Mitochondrial NADH Dehydrogenase Subunit 5 and NADH Dehydrogenase Subunit 4 Genes in the Chagas Disease Vector Triatoma infestans (Hemiptera: Reduviidae)

“…5 The mitochondrial NADH dehydrogenase subunit 5 (ND5) and NADH dehydrogenase subunit 4 (ND4) are two of the most variable protein-coding genes in insects. [6][7][8] We tested variation of the ND5 and ND4 genes in individual T. infestans from 24 localities in Argentina.…”