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Erik Andersen

· Professor & Vice Chair, Department of BiologyVerified

Johns Hopkins University · Genetics and Molecular Biology

Active 1968–2026

h-index46
Citations8.3k
Papers214130 last 5y
Funding$12.0M1 active
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About

Erik Andersen is a geneticist with extensive experience in molecular, quantitative, and population genetics and genomics. He received his B.S. in Biological Sciences from Stanford University, where he was awarded the Firestone Medal for Excellence in Research. He earned his Ph.D. at the Massachusetts Institute of Technology, studying developmental genetics of chromatin remodeling in Caenorhabditis elegans under the advisement of Dr. H. Robert Horvitz. His research interests shifted to quantitative genetics and genomics during his NIH NRSA Post-doctoral and Howard Hughes Medical Institute Fellowship with Dr. Leonid Kruglyak at Princeton University. From 2013 to 2023, his work at Northwestern University focused on understanding the genes and molecular mechanisms underlying phenotypic differences in evolutionary genetics, utilizing large-scale genetics and genomics studies in nematodes as model animals. His laboratory created extensive collections of wild strains for multiple nematode species to explore questions of evolutionary relevance, including molecular interactions in epistasis and niche preferences in nature. His contributions span genetic, genomic, physiological, systems, and ecological perspectives. In 2023, his laboratory moved to Johns Hopkins University to further research in genetics and genomics in Caenorhabditis and other nematode species, including efforts to establish new model parasitic nematode species to investigate drug resistance and host-pathogen biology.

Research topics

  • Genetics
  • Biology
  • Computational biology
  • Ecology
  • Evolutionary biology
  • Biochemistry
  • Toxicology
  • Zoology
  • Chemistry
  • Pharmacology

Selected publications

  • Methods for single-pair Ascaridia galli genetic crosses

    PubMed · 2026-02-02

    articleOpen accessSenior author

    , a common ascarid of chickens. Sexually immature larval parasites were recovered from donors, transferred to gelatin capsules, and then given orally to recipients. We successfully established single-pair matings in 32% of crossing attempts. This method to control genetic crosses further establishes the avian model for ascarid research and will enable future studies to create a high-quality reference genome, inbreed anthelmintic resistant and sensitive lines, and investigate host-pathogen interactions.

  • Global genomic diversity of the selfing nematode Caenorhabditis tropicalis correlates with geography

    bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-08

    articleOpen accessSenior author

    Self-fertilization reduces genetic diversity compared to outcrossing and hypothetically decreases the ability to adapt to diverse environments. Among Caenorhabditis nematodes, self-fertilization evolved three times independently in Caenorhabditis elegans, Caenorhabditis briggsae, and the more recently discovered Caenorhabditis tropicalis. To survey C. tropicalis genetic relatedness, the influence of geography and niche on species-wide variation, and the signatures of selection, we collected 785 wild strains, sequenced their genomes, and identified 622 distinct genotypes (isotypes). In contrast to C. elegans and C. briggsae, C. tropicalis relatedness shows substantial association with geography and no transcontinental selective sweeps or broadly sampled isotypes. Populations from the Hawaiian Islands or Taiwan harbor more genetic variation than populations from the Caribbean or Americas, suggesting a Pacific species origin similar to other members of the Elegans subclade. Punctuated genomic regions of extreme genetic variation pervade the genome. These hyper-divergent regions (HDRs) comprise less than 6% of the reference genome in any given strain despite harboring 73% of all variant sites and are enriched for genes likely involved in environmental adaptation. HDRs represent a shared genomic feature of self-fertilizing Caenorhabditis nematodes despite their independent evolutionary origins and suggest a mechanism to explain worldwide distributions despite low species-wide levels of genetic variation.

  • Natural variation suggests candidate genes underlying <i>Caenorhabditis elegans</i> susceptibility to diverse toxicants

    Toxicological Sciences · 2026-02-17

    articleOpen accessSenior author

    Genetic differences among individuals shape how they respond to environmental toxicants, but the identification and validation of the genes responsible for this variation is difficult, particularly in humans. Consequently, our limited knowledge of the genes that influence susceptibility constrains our ability to accurately predict the risks posed by environmental toxicants. To identify genes underlying natural differences in toxicant susceptibilities, we measured the effects of 23 environmental toxicants on larval development across 195 genetically diverse Caenorhabditis elegans strains using a high-throughput imaging platform. We then combined these response data with whole-genome sequences to perform genome-wide association mappings, identifying 40 genomic regions where genetic variants are correlated with susceptibility differences. Many of these regions are enriched for genes involved in biological processes previously linked with toxicant responses, supporting the potential contributions of these genes to natural variation in susceptibility. Using biologically informed heuristics based on genomic context and functional annotation, we prioritized genes for follow-up experimentation and identified 94 candidate susceptibility genes, offering feasible targets for experimental validation that could ultimately inform toxicant risk prediction and regulatory assessment by linking genetic variation to differences in susceptibility. Analysis of natural genetic variation among 195 wild C. elegans strains identified 94 candidate genes putatively linked to differences in susceptibility to 23 environmental toxicants. These findings can inform the discovery of conserved susceptibility genes and the development of biomarkers that improve chemical risk assessment by accounting for genetic differences among humans.

  • Evolution of the rate, molecular spectrum, and fitness effects of mutation under minimal selection in <i>Caenorhabditis elegans</i>

    Genetics · 2026-03-26

    article

    The rate, molecular spectrum, and fitness effects of mutations vary at all levels of the biological hierarchy, from within individual genomes to among taxonomic domains. Understanding the evolutionary factors underpinning that variation is of fundamental importance to biology. Accurate quantification of the properties of mutations requires that other evolutionary forces, especially natural selection, be minimized as much as possible. To investigate the evolution of the mutational process in Caenorhabditis elegans, we propagated a set of 100 "first order" mutation accumulation (O1MA) lines under minimal selection for ∼150 generations, divided each O1MA line into 2 "second order" MA (O2MA) lines and propagated them for another ∼150 generations, at which time the genome of each O2MA line was sequenced, and a subset of 50 O1MA families was assayed for competitive fitness. Over the course of the experiment, the mean nucleotide substitution mutation rate did not change, but the variance increased. In contrast, the indel mutation rate increased significantly. The 2 types of mutations fulfill the predictions of different theoretical models for the evolution of mutation rate. These results reinforce previous findings that the rate of indels is more sensitive to endogenous stress than the rate of nucleotide substitutions. Several evolutionary quandaries could be resolved if deleterious mutations interact synergistically (negative epistasis). Evidence for synergistic epistasis is famously inconclusive, although there is reason to think it may be more detectable under competitive conditions. However, a model of constant mutational effects on competitive fitness explains the results significantly better than a model including epistasis.

  • A gap-free, telomere-to-telomere genome assembly for the <i>Caenorhabditis briggsae</i> reference strain AF16

    bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-04

    articleOpen accessSenior authorCorresponding

    The nematode Caenorhabditis elegans was the first metazoan to have its genome completely sequenced and assembled. Since that time, researchers have continuously updated the reference genome and manually curated its approximately 20,000 genes. The closely related species, Caenorhabditis briggsae , has served as a comparative model because of its similar morphology, mode of reproduction, and patterns of intra-species genetic variation. However, the genomic resources for C. briggsae lag behind C. elegans , hindering comparative genomics studies between the species. Decades of experimentation have been performed in the AF16 reference strain genetic background, so we obtained high-coverage long-read sequencing and high-throughput chromosome conformation capture data to create an updated reference genome for an isogenic derivative of AF16, named CGC2. The CGC2 genome is vastly improved relative to the existing AF16 assemblies, with no unplaced sequence, no gaps, and telomere-to-telomere contiguity. To provide genomic resources for CGC2, we exploited deep RNA-seq libraries from all developmental stages to predict protein-coding gene annotations comparable in accuracy and completeness to the existing AF16 gene models. We also performed lift-over of 108 validated insertion-deletion variants to the updated coordinate system of the CGC2 genome to facilitate future mappings of mutations. In summary, we present an updated reference genome for the canonical AF16 reference strain with improved genomic resources to enable high-quality intra- and inter-species comparative studies.

  • Mutational divergence over years in local populations of the selfing nematode <i>Caenorhabditis elegans</i>

    Genetics · 2026-02-17

    article

    Laboratory mutation accumulation experiments allow the assessment of spontaneous mutation rates and patterns with minimal selection. Here, we aimed to follow the accumulation and fate of mutations in natural populations, in a spatial context. The nematode Caenorhabditis elegans is particularly suited for such endeavor, as it reproduces almost exclusively by selfing. We analyzed the evolution of clonal C. elegans genotypes along a 300-m-long stream bank in the Santeuil wood (France), based on short-read whole-genome sequencing of individuals collected between 2009 and 2022. We monitored along years the evolution of two of these quasi-clones, composed of individuals only differing by recent mutations. Recombination was scarce. A temporal signal was detected: strains from earlier years were found close to inner nodes of the tree, while recent ones were found on outer tips. This signal allowed us to estimate a substitution rate of 4 to 5 × 10-8 mutations per base pair per year, which can be used to calibrate divergence times among and within species. Mutation densities were higher on the X chromosome, on chromosome arms, and in non-exonic regions. We detected a high transition-to-transversion ratio, not observed in C. elegans laboratory mutation accumulation lines. Based on the spontaneous mutation rate per generation in laboratory lines of intergenic regions under minimal purifying selection, we estimated that C. elegans locally undergoes around 25 effective generations per year. Finally, using these recent mutations, we detected a spatiotemporal pattern within the field site, indicating limited dispersal at the scale of 100 m within 10 years.

  • Survey of benzimidazole resistance in ascarid parasites of poultry

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-12

    preprintOpen accessSenior authorCorresponding

    ABSTRACT Ascarid parasites, such as Ascaridia galli and Heterakis gallinarum , are nearly ubiquitous in poultry and can cause serious production losses. H. gallinarum is of particular concern because of its role as a vector for the protozoan Histomonas meleagridis , the cause of blackhead disease. Currently, only the benzimidazole anthelmintic, fenbendazole (FBZ), is approved for use in poultry, and recently, FBZ resistance has been discovered and validated in populations of the turkey ascarid Ascaridia dissimilis and in ascarid of gallinaceous birds H. gallinarum . Here, we further explore the prevalence of resistance in poultry ascarids by testing FBZ efficacy against thirteen isolates of A. galli and eight isolates of H. gallinarum . Isolates were used to infect day-old naive chickens. Four weeks after infection, animals to be treated received the label-recommended dosage of FBZ (SafeGuard Aquasol) for five days, per the manufacturer’s directions. One week after the fifth day of treatment, animals were euthanized and parasite burdens were counted to determine treatment efficacy between the untreated and treated groups. Resistance was identified and validated in a single isolate of A. galli , marking the first confirmed case in the species. All isolates of H. gallinarum were found to be resistant. The emergence of resistance in A. galli and the high prevalence of resistance in H. gallinarum highlight the growing concern of resistance in parasites of poultry. Without approved alternative treatments, the detrimental effects of infections cannot be mitigated in resistant populations, significantly impacting profit margins. Diagnostics that enable broader surveys are necessary to understand the full scope of the problem. However, we show that resistance is present across production species and should act as an impetus for the discovery of new treatments and the adoption of new management strategies.

  • <i>Caenorhabditis briggsae</i> ancestral genomic hyper-diversity contrasts with globally distributed genome-wide haplotypes

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-11 · 2 citations

    articleOpen accessSenior authorCorresponding

    Comparative genomics provides a powerful framework to uncover the molecular and evolutionary mechanisms that shape genetic diversity within and across species, revealing how shared and lineage-specific processes influence their evolutionary trajectories through time. The nematode Caenorhabditis briggsae is distributed world-wide and is a comparative model to Caenorhabditis elegans in the biology of development, cellular mechanisms, neurobiology, genetic mappings of complex traits, and genome evolution. Following massive collection efforts by the nematode research community, we present the isolation of over 2,000 wild strains and analyses of genome sequences that catalog over six million single-nucleotide and insertion-deletion variants. This genome and strain resource provide a powerful means to interrogate the causal genetic bases of phenotypic variation for diverse traits. Additionally, we describe its global population structure and discover new and genetically distinct groups within this primarily self-fertilizing species, including groups of highly related strains that were sampled across different continents. We leverage expansive genetic variation to decipher the effects of linkage and selection on the distribution of genetic diversity across the genome and across geographic regions. Within the species, we find genomic regions with extremely high levels of genetic variation similar to hyper-divergent regions found in C. elegans and other species. These regions harbor new genes and variation enriched for environmental sensing and pathogen responses. In comparison to the outbreeding sister species Caenorhabditis nigoni , we conclude that long-term balancing selection has maintained substantial functional variation since the divergence from their outbreeding ancestor, likely in response to differences in the ecological niche. Overall, this massive strain resource enables future comparative genetics and genomics studies, including genome-wide association studies between Caenorhabditis species.

  • High-throughput developmental assay of cold tolerance in <i>Caenorhabditis elegans</i>

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-16

    preprintOpen access

    Abstract Temperature can impose strong selection causing thermal tolerance variation between individuals, populations, and species. We developed a high-throughput larval development assay for cold tolerance in the model organism Caenorhabditis elegans . We exposed animals to 4°C cold treatments for either 12 or 24 hours. Animals exposed to the 24-hour cold treatment exhibited greater variation and heritability in cold tolerance during the L1 larval stage. The high-throughput approach that we developed is easily scalable to simultaneously measure a large number of strains, which makes it ideal for studying the genetics and evolution of cold tolerance in Caenorhabditis nematodes.

  • Independent mechanisms of benzimidazole resistance across <i>Caenorhabditis</i> nematodes

    bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-15

    preprintOpen accessSenior authorCorresponding

    ABSTRACT Benzimidazoles (BZs), a widely used class of anthelmintic drugs, target beta-tubulin proteins, disrupt microtubule formation, and cause nematode death. In parasitic nematode species, mutations in beta-tubulin genes ( e.g. , isotype-1 beta-tubulin) are predicted to inhibit BZ binding and are associated with BZ resistance. Similarly, in the free-living nematode Caenorhabditis elegans , mutations in an isotype-1 beta-tubulin ortholog, ben-1 , are the primary drivers of BZ resistance. The recurrent association of BZ resistance with beta-tubulins suggests that BZ resistance is repeatedly caused by mutations in beta-tubulin genes, an example of repeated evolution of drug resistance across nematode species. To evaluate the hypothesis of repeated evolution of BZ resistance mediated by beta-tubulin, we identified predicted resistance alleles in beta-tubulin genes across wild strains from three Caenorhabditis species: C. elegans , Caenorhabditis briggsae , and Caenorhabditis tropicalis . We hypothesized that, if these species experienced similar selective pressures, they would evolve resistance to BZs by mutations in any of three beta-tubulin genes ( ben-1 , tbb-1 , and tbb-2 ). Using high-throughput development assays, we tested the association of predicted beta-tubulin alleles with BZ resistance. We found that a heterogeneous set of variants identified in C. elegans ben-1 were associated with BZ resistance. In C. briggsae , only two variants in ben-1 , predicted to encode a premature stop codon (W21stop) and a missense substitution (Q134H), were associated with BZ resistance. In C. tropicalis , two missense variants were identified in ben-1 , but neither was associated with BZ resistance. C. briggsae and C. tropicalis might have evolved BZ resistance by mutations in other beta-tubulin genes, but we found that variants in tbb-1 or tbb-2 in these species were not associated with BZ resistance. Our findings reveal a lack of repeated evolution of BZ resistance across the three Caenorhabditis species and highlight the importance of defining BZ resistance mechanisms outside of beta-tubulins.

Recent grants

Frequent coauthors

  • Stefan Zdraljevic

    University of California, Los Angeles

    41 shared
  • Robyn E. Tanny

    Johns Hopkins University

    35 shared
  • Timothy A. Crombie

    Northwestern University

    34 shared
  • Christian Braendle

    Institut de Biologie Valrose

    32 shared
  • Daniel E. Cook

    Google (United States)

    32 shared
  • Daehan Lee

    Northwestern University

    27 shared
  • Kathryn S. Evans

    Northwestern University

    26 shared
  • Gaotian Zhang

    Université Paris Sciences et Lettres

    25 shared

Labs

Awards & honors

  • Pew Biomedical Scholar
  • National Science Foundation CAREER recipient
  • Fulbright Global Scholar recipient
  • American Cancer Society Research Scholar
  • Human Frontiers Science Program Grantee
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