Figure 1.
Examples of two misassembled scaffolds.
Individual contigs are shown as gray rectangles. Contigs with markers in this study are indicated with an * above the scaffold and are labeled with their position on the genetic map. The new scaffolds created by splitting misassemblies (identified in this study only) are shown with solid lines. New scaffolds with suffixes ‘a,’ ‘b,’or ‘c’ contain markers that allow placement on the genetic map. New scaffolds with suffixes ‘m’ or ‘n’ fall between conflicting markers and therefore contain a misassembly and cannot be placed on the genetic map. A) Supercontig 1.1 with markers from the previously published integrated map [20] shown below. The mapping of markers to two different chromosomes indicates a misassembly within the scaffold, which is supported by both markers sets. B) Supercontig 1.48 with synteny with An. gambiae shown below the scaffold and the different colors indicating different chromosome arms. Both our markers and syntenic breaks with An. gambiae indicate that this scaffold is misassembled in at least two instances.
Figure 2.
The map was constructed using SNPs identified in RAD tag sequences. Positions in cM are indicated to the left of each linkage group. Scaffolds mapping to each position on the map are shown to the right of each linkage group and are named by the last 2–4 digits of their supercontig ID number. The region linked with resistance to infection by B. malayi is highlighted in red. Scaffolds with suffixes a–d were previously misassembled and have been split and assigned new scaffold names (see Figure 1 and Table S2 for additional information).
Table 1.
Summary of our assembly of the genome onto a genetic map.
Figure 3.
The correlation between the cM position of a scaffold on our genetic map and its position on the previously published integrated map [20].
The positions of scaffolds on chromosomes 1 (A), 2 (B), and 3 (C) are significantly correlated between the map presented here and the previously published map order (Spearman correlation, A: ρ = 0.803, P = 0.0017; B: ρ = 0.899, P = 0<0.0001; C: ρ = 0.857, P = 0.0004). Outliers are potentially caused by unidentified scaffold misassemblies. In cases where we found a scaffold to be misassembled, the correlation was performed by using the genetic map position of the contig closest to the one used in [20]. In one instance on Chromosome 2 and two instances on Chromosome 3, scaffolds mapped to a different chromosome in [20] than on our genetic map and these are not included in this analysis.
Figure 4.
Synteny between the chromosomal arms of Ae. aegypti and An. gambiae can be used to corroborate scaffold misassemblies in Ae. aegypti.
A) Synteny is maintained between chromosomal arms in Ae. aegypti and An. gambiae. Each square represents a 1∶1 orthologous gene (>70% identity) between species. The position is plotted as the centimorgan position on the genetic map for Ae. aegypti and the base pair position along the chromosomal arm in An. gambiae. The solid line at the bottom illustrates the syntenic relationships that have previously been observed [11]. B) Misassemblies are supported by breaks in synteny in cases where both halves of a misassembled scaffold have orthologous genes in An. gambiae. Each point along the x-axis represents a contig with an ortholog in An. gambiae and its location on the y-axis represents its position in An. gambiae. Dotted line represents scaffold misassembly breakpoints that were detected using the genetic map.
Figure 5.
The relationship between genetic (cM) and physical map (Mb) positions and estimated local recombination rates across the three chromosomes of Ae. aegypti.
The physical length was measured as the number of base pairs mapped to a particular genetic position for chromosomes A) 1, B) 2, and C) 3. Local recombination rates for chromosomes D) 1, E) 2, and F) 3 show depressed recombination in the centromeric regions of each chromosome.
Figure 6.
Resistance to B. malayi is determined by a single locus that is dominant in action and maps to the first chromosome.
A) Average frequencies of the reference allele (the SNP allele in the published genome) in the pools of refractory versus susceptible mosquitoes. A cluster of markers with ∼100% frequency in susceptible pools (vertical dotted lines) and ∼50% frequency in refractory pools (horizontal dotted line) is consistent with resistance being determined by a single locus that is dominant in action. Red points indicate statistically significant differences in allele frequencies between refractory and susceptible pools at a genome-wide significance of P<0.01. B) Manhattan plot of the minimum P-values for each scaffold, with the x-axis representing a physical map created from the linkage map. Only markers from contigs used to assemble the linkage map are shown here (see Table S2). Dotted line indicates significance at a genome-wide significant of P<0.01.