Philipp W. Messer

This study develops a modeling framework for gene drives in plants that includes soil seedbanks, showing how seedbanks can slow spread but reduce genetic load and provide biosafety.

The paper introduces e3SIM, a simulator that models epidemiological, ecological, and evolutionary processes in pathogens, demonstrating its use with SARS-CoV-2 and Mycobacterium tuberculosis.

SLiM 5 extends the simulation framework to support multiple chromosomes, enabling full-genome simulations with various chromosome types.

This study investigates the invasion dynamics of threshold-dependent gene drives in spatially structured populations using reaction-diffusion models and individual-based simulations, revealing complex spatial containment behaviors.

The paper introduces a SLiM 5 model for simulating whole-genome human evolution, including sex chromosomes and mitochondrial DNA, and demonstrates its utility through simple analyses.

This study simulates selective sweeps in spatially structured populations and finds that low dispersal leads to distinct genetic signatures, including reduced diversity and intermediate-frequency variants.

This paper provides a guide to implementing individual-based simulations in continuous landscapes, focusing on population dynamics and ecological applications.

This study investigates when spatial structure should be included in epidemiological models and derives a critical threshold for diffusion coefficient affecting disease spread predictions.

This paper introduces a resource-explicit modeling method for spatial population models that improves computational efficiency while maintaining accuracy.

This study analyzes spatial suppression gene drive dynamics, finding that larger areas and certain life history traits increase vulnerability to chasing, while resistance mechanisms affect drive performance.

This paper presents a framework to identify fertility gene targets for mammalian pest control by evaluating gene function, expression, and knockout results, identifying 16 male and 12 female fertility genes conserved across invasive species.

The paper identifies new germline Cas9 promoters in Drosophila that improve drive conversion efficiency while reducing embryo resistance and somatic expression.

The paper simulates two Anopheles homing gene drives and finds the combined drive with X-shredder is less effective than drives using the nos promoter.

This paper develops a homing suppression gene drive in Drosophila using multiplexed gRNAs to prevent resistance alleles, achieving high conversion efficiency and moderate population suppression.

The paper evaluates a buffering mechanism for deleterious mutations and shows it leads to lower adaptive fixation rates and reduced MK test power compared to an arms race model.

This paper develops a theoretical framework to predict the genomic resolution of bulk segregant analysis (BSA) based on coalescence theory and experimental parameters.

This paper demonstrates a tethered gene drive system in Drosophila that confines homing drives to target populations, enabling controlled modification or suppression.

This study simulates CRISPR-based underdominance gene drives using toxin-antidote principles to assess their performance and confinability in population modification and suppression.

This paper presents a CRISPR homing gene drive in Drosophila that reduces resistance allele formation by targeting a haplolethal gene, achieving high efficiency in allele spreading.

The paper evaluates CRISPR-based toxin-antidote gene drive systems to assess their resistance resistance and regional confinement capabilities for population modification and suppression.

This study examines underdominance gene drive systems in continuous space, finding that they may fail to persist and can spread to neighboring populations despite local confinement.

The paper models CRISPR homing gene drives with multiple gRNAs, finding optimal gRNA numbers and showing their limited standalone effectiveness but value when combined with other strategies.

The paper introduces a CRISPR gene drive system called TARE that limits resistance and spreads regionally in Drosophila.

The paper investigates how natural genetic variation affects resistance to CRISPR gene drives in Drosophila, finding that resistance rates vary widely and are polygenic with small-effect loci.

The paper demonstrates synthetic target sites and split drives as safeguarding strategies to prevent unintended spread of CRISPR gene drives from lab to natural populations.

This study evaluates strategies to reduce resistance allele formation in CRISPR gene drives, finding that using the nanos promoter, adding a second gRNA, and using an autosomal male germline drive can lower resistance rates.

The paper models the Mutagenic Chain Reaction (MCR) as a meiotic drive mechanism, showing that an introduced allele can invade a population only if its frequency exceeds a critical threshold, even when it has a fitness cost.