Six published papers and one preprint from 2026 that were missed in last round of updates are covered here.
Sex determination and the evolution of selfing
The third route to self-fertility looks nothing like the first two. Kennedy et al. have examined sex determination in C. tropicalis, one of the three Caenorhabditis species to have evolved hermaphroditism independently. The core pathway genes act in the same order in the soma of all three species, but C. tropicalis departs from every Caenorhabditis studied so far: tra-2 XX mutants resemble tra-1 XX mutants rather than differing in tail development, and neither gene controls the male behaviors that the pathway governs elsewhere. Germ cell fate follows a simple linear process seen in neither C. elegans nor C. briggsae.
Epistasis experiments showed that in all three species the sperm-to-oocyte switch in XX hermaphrodites occurs at the level of tra-2. Three independent origins converging on the same control point suggests that node is unusually accessible to regulatory change. Note that the Ellis lab also authored the Haldane’s rule paper covered in last week’s updates.
Kennedy et al. (2026), GENETICS 233(4):iyag145
Natural variation and drug resistance
Benzimidazole resistance is far more constrained in C. briggsae than in C. elegans. Shaver et al., from the Andersen lab, tested every wild strain carrying variants in the five conserved beta-tubulin genes (tbb-1, tbb-2, mec-7, tbb-4 and ben-1) across C. elegans, C. briggsae and C. tropicalis. In C. elegans a heterogeneous set of ben-1 variants conferred resistance. In C. briggsae, only two did: W21stop and Q134H. In C. tropicalis, no strain carrying a variant in any beta-tubulin gene was resistant.
Since C. briggsae and C. elegans have overlapping geographic ranges, the contrast argues that selection on this locus differs between the two species rather than tracking shared exposure. The authors also generated CRISPR–Cas9 ben-1 deletions in the AF16 and NIC58 backgrounds, which serve as useful reagents.
Shaver et al. (2026), PLoS Pathogens 22(6):e1014306
Pathogens and microbiota
A new fungal pathogen of Caenorhabditis, spotted first in wild C. briggsae. Ni et al. at West Chester University identified Mucor hiemalis in the intestinal lumen of wild C. briggsae. They then confirmed infection by co-culturing with reporter C. elegans. The fungus kills its host by perforating the intestine. Nematodes actively prefer food containing M. hiemalis sporangiospores, and infection induces genes belonging to the intracellular pathogen response.
The pool of natural Caenorhabditis pathogens is small so each addition is worth knowing about, and this one surfaced in C. briggsae first.
Ni et al. (2026), Infection and Immunity 94(5):e00310-25
No vertically transmitted endosymbionts found in over 4,000 wild strains of three free-living self-fertilizing Caenorhabditis species . A study from the Andersen and Luallen labs took unaligned sequencing reads from 1,790 C. briggsae, 1,631 C. elegans and 690 C. tropicalis strains in CaeNDR release 20231201 and classified them with Kraken2. After filtering laboratory and ubiquitous environmental genera, 321 C. briggsae strains (17.9%) still carried classifiable non-Caenorhabditis sequence. None of it belonged to Rickettsia, Wolbachia or Ehrlichia, even at a relaxed 4% minimizer threshold, and FISH probing of selected strains produced no experimental evidence of intracellular residents.
A clean, well-powered negative result, and a useful one.
O’Connor et al. (2026), microPublication Biology
The same glycosyltransferase mutates to antiviral resistance in two species independently. A preprint from the Félix lab (includes Gaotian Zhang as a co-corresponding author) maps the major resistance locus of the C. elegans strain MY10 to a rare non-synonymous polymorphism in gtnt-1, encoding a putative GT92-family glycosyltransferase. Resistance through gtnt-1 has arisen repeatedly in C. elegans, with each allele sitting below 1% frequency. Turning to C. briggsae strains differing in viral susceptibility, the authors show that hypomorphic alleles of Cbr-gtnt-1 likewise impair infection and improve host fitness under it.
Two species, the same gene, the same direction of effect, and in both cases the resistant alleles stay rare, leading authors to read as transient adaptation in a shifting eco-evolutionary context rather than a sweep.
Richaud et al. (2026), bioRxiv 2026.04.14.718442
Stress and lifespan
Cbr-hsf-1 is required for normal lifespan, but not for acute stress survival. Bhullar et al. (from our lab) used RNAi knockdown of Cbr-hsf-1 to separate the two roles. Knockdown from embryogenesis to Day 1 adulthood reduced mean lifespan by ~25% both at 20 °C and 30 °C. However, the population declined faster at the higher temperature based on time to 90% mortality that fell 33% at 30 °C against 17% at 20 °C. Knockdown started at Day 1 of adulthood also shortened lifespan, providing evidence for Cbr-hsf-1 requirements during adulthood. Interestingly, Cbr-hsf-1 RNAi-treated animals survived 35 °C acute heat shock and 24-hour ER stress no worse than controls.
Bhullar et al. (2026), microPublication Biology
Elsewhere
C. briggsae turns up in an Australian biosecurity screen. A CSIRO proof-of-concept study applied RNA-sequencing (RNA-seq) to 60 native and introduced land snails collected near major Australian ports, and recovered C. briggsae transcripts from the introduced snail Paropeas achatinaceum.
The methodological warning is worth mentioning: candidate hits against the curated 18S NemaBase turned out to be probable mis-assignments once checked against the much broader NCBInt, which had closer matches. Worth remembering if you are assigning nematode identities from a specialist database alone.
Talamantes-Becerra et al. (2026), Infection, Genetics and Evolution 139:105898
Corrections and additions are welcome.