Andrea Crisanti

This study investigates the role of the femaleless gene in Anopheles gambiae gametogenesis and its impact on CRISPR-Cas9 gene drive efficacy, showing that disrupting fle causes female sterility and limits gene drive spread.

This paper proposes a self-limiting gene drive strategy called MDFS to suppress malaria mosquito populations by causing female sterility while allowing fertile males to spread the trait.

The paper investigates sex-specific hearing in mosquitoes by analyzing the role of a female-specific isoform of the doublesex gene and its impact on auditory function.

The paper introduces a Y chromosome-linked genome editor (YLE) for population suppression in Anopheles gambiae, showing it is up to 8 times more efficient than other self-limiting strategies.

The paper presents a pipeline to discover and engineer gene drives that overcome resistance in malaria mosquitoes, showing that new resistant alleles can emerge and designing drives that target multiple sites to suppress populations.

This study uses CRISPR/Cas9 to target the Y chromosome in Anopheles gambiae, causing meiotic defects and a female-biased progeny, providing insights into synthetic sex ratio distortion mechanisms.

The paper evaluates resistance to a CRISPR-based gene drive by simulating high selection pressure in Anopheles gambiae and identifies a resistant mutation at an ultra-conserved site.

The paper identifies ultra-conserved sequences in Anopheles mosquito genomes and suggests their potential use as targets for gene drive-based malaria control.

This study improves gene drive efficacy by reducing resistance and fitness costs through regulatory sequence modifications, leading to better population suppression and delayed resistance.

The paper demonstrates that Y chromosomes from two malaria vector species in the Anopheles gambiae complex function interchangeably, suggesting no hybrid incompatibility loci on the Y and enabling potential cross-species sex-distorting Y drive interventions.