Resistance to <i>B</i>. <i>malayi</i> is dominant and sex-linked, and it impairs early stages of <i>B</i>. <i>malayi</i> development.

Abstract

<p>Female progeny from a backcross inherited the resistance phenotype of their maternal grandparent, whether resistance was measured as A) the proportion of mosquitoes infected with L3 stage parasites or B) the number of L3 stage parasites at 10 days after infection. S♀ x R♂ (referred to as susceptible from this point forward) were created by crossing an LVP<sup>S</sup> female with an LVP<sup>R</sup> male, followed by backcrossing the F<sub>1</sub> progeny to LVP<sup>S</sup>. R♀ x S♂ (referred to as resistant) were created in the same way except an LVP<sup>R</sup> female was crossed with an LVP<sup>S</sup> male in the parental generation. By 24 hours after infection, many <i>B</i>. <i>malayi</i> microfilariae have migrated from the midgut to the thoracic tissues in both C) susceptible and D) resistant hosts. At 48 hours after infection, microfilariae are molting into the non-feeding L1 developmental stage in E) susceptible hosts, whereas growth is arrested in F) resistant hosts. By 72 hours after infection, nearly all surviving <i>B</i>. <i>malayi</i> are in the L1 stage in G) susceptible hosts, whereas they are dead or dying in H) resistant hosts. I) Genome-wide gene expression levels of <i>B</i>. <i>malayi</i> are comparable in resistant and susceptible hosts at 12 hours after infection, whereas by 48 hours, gene expression, and presumably growth, of <i>B</i>. <i>malayi</i> is higher in susceptible mosquitoes. <i>B</i>. <i>malayi</i> gene expression is estimated by dividing the total number of RNA-seq reads mapping to the <i>B</i>. <i>malayi</i> genome by the total number of reads mapping to the <i>Ae</i>. <i>aegypti</i> genome.</p

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