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Ragsdale, E. J.

Publications and source records attributed to Ragsdale, E. J..

3 recordsLinked to original sources

Hidden in the genomic bycatch: insights into genome reorganization and population structure of the parasitic nematode Contortylenchus reversus

Insect-parasitic nematodes are widespread and often significantly reduce host fitness, yet we know surprisingly little about most species. Contortylenchus reversus is a hemocoel-inhabiting parasitic nematode that infects Dendroctonus bark beetles, notably impacting host mobility and fecundity. We first detail a chromosome-scale genome assembly of C. reversus, recovered serendipitously from a sequencing project targeting a host (Dendroctonus ponderosae). We assembled the 79.4 Mb genome into nine linkage groups and, through transcriptome-aided annotation, identified 11,244 protein-coding genes. Synteny comparisons with the only relatives for which there are complete assemblies reveal extensive chromosomal rearrangements and extreme loss of gene collinearity suggesting these insect-parasitic nematodes may have exceptionally malleable genomes. Using this genome assembly and repurposed reduced-representation genomic data from 707 D. ponderosae individuals, we investigated infection frequencies and population structure, identifying infection rates ranging from 0% to 50% across 18 geographically widespread collection sites. Population structure of C. reversus appears broadly concordant with the structure of the host beetle, suggesting a shared evolutionary history, while genetic variation (nucleotide diversity) in the parasitic nematode is highly reduced in comparison to its host. These results offer insights into its population genetics, host associations, and the evolutionary dynamics of a nematode-beetle interaction and highlight how genomic bycatch can reveal previously hidden details about an important species in a complex community.

genomics↗

Three-dimensional reconstruction of the face and feeding apparatus of the predatory nematode Pristionchus pacificus

Pristionchus pacificus is a nematode model for the developmental genetics of morphological polyphenism, especially at the level of individual cells. Morphological polyphenism in this species includes an evolutionary novelty, moveable teeth, which have enabled predatory feeding in this species and others in its family (Diplogastridae). From transmission electron micrographs of serial thin sections through an adult hermaphrodite of P. pacificus, we three-dimensionally reconstructed all epithelial and myoepithelial cells and syncytia, corresponding to 74 nuclei, of its face, mouth, and pharynx. We found that the epithelia that produce the predatory morphology of P. pacificus are identical to Caenorhabditis elegans in the number of cell classes and nuclei. However, differences in cell form, spatial relationships, and nucleus position correlate with gross morphological differences from C. elegans and outgroups. Moreover, we identified fine-structural features, especially in the anteriormost pharyngeal muscles, that underlie the conspicuous, left-right asymmetry that characterizes the P. pacificus feeding apparatus. Our reconstruction provides an anatomical map for studying the genetics of polyphenism, feeding behavior, and the development of novel form in a satellite model to C. elegans.

zoology↗

Evolution of developmental plasticity by opposing dosage of signalling-modifying enzymes

Polyphenism, the extreme form of developmental plasticity, is the ability of a genotype to produce discrete morphologies matched to alternative environments. Because polyphenism is likely to be under switch-like molecular control, a comparative genetic approach could reveal the molecular targets of plasticity evolution. In the nematode Pristionchus pacificus, which form two alternative feeding-morphs, the polyphenism threshold is set by relative dosage of two lineage-specific enzymes that respond to morph-inducing cues. One enzyme, the sulfotransferase SEUD-1, integrates an intercellular signalling mechanism at its ultimate target, the cells producing dimorphic mouthparts. Additionally, multiple alterations of seud-1 support it as a potential target for plasticity evolution. First, a recent duplication of seud-1 in a sister species reveals a direct correlation between genomic dosage and the polyphenism threshold. Second, laboratory selection on the polyphenism threshold resulted in changes in relative transcriptional dosage. Our study thus offers a genetic explanation for how plastic responses evolve.

evolutionary biology↗