Sunita B. Sumanam

The evolutionary transition from free-living bacteria to host-adapted symbionts is typically accompanied by substantial genomic changes. Within the genus Serratia , this transition has so far been documented only in the aphid-associated species, Serratia symbiotica , whereas all other Serratia species are free-living. In this study, we identify a putatively new Serratia taxon using metagenomic approaches in the trombidiform mite, Halotydeus destructor . We provide genomic evidence for a possible transition to a host-adapted lifestyle in this new Serratia sp., which sits phylogenetically within a clade of free-living Serratia species. The genomic signatures of evolving toward a host-adapted lifestyle include a reduced genome size and coding capacity, an elevated transposase fraction, and detectable chromosomal rearrangements, relative to other free-living Serratia species. However, the species does not show the same structure of genome reduction as S. symbiotica . Functional gene content analyses including COG categories and virulence factor repertoires also showed that our new Serratia sp. had a distinct gene profile from both free-living Serratia and S. symbiotica . Additional genomic screening suggests that infections of the new Serratia sp. are common in wild populations of H. destructor across its invasive Australian range, warranting future investigations on the possible role this symbiont plays in the evolutionary ecology of its mite host. Our work not only highlights a potential parallel transition to a host-adapted lifestyle in the Serratia genus, but also represents the first characterisation of a possible host-adapted Serratia taxon in a trombidiform mite.

The redlegged earth mite, Halotydeus destructor , is an invasive pest of grain and pasture crops in Australia. Australian populations are increasingly developing resistance to broad‐spectrum pesticides. Here, we assembled a chromosome‐level genome for H. destructor , comprising nine chromosomes and totalling approximately 46 Mb. We also generated a genomic dataset from 190 populations collected across thousands of kilometres of its invasive Australian range and across 4 years (2018, 2021, 2022 and 2023), and used this dataset to develop KASP (Kompetitive allele‐specific PCR) markers for identifying resistance mutations. We combined pooled whole‐genome sequencing with resistance testing for organophosphate pesticides, chlorpyrifos and omethoate, and the pyrethroid pesticide, bifenthrin. Target‐site resistance to chlorpyrifos was strongly associated with the common ace G119S mutation. A second mutation, ace A201S, was also common, although its association with chlorpyrifos or omethoate resistance was less clear. Target‐site resistance to bifenthrin was strongly associated with the common para L1024F mutation. We also detected several rare target‐site mutations that likely contribute to resistance in specific populations, including F331Y in ace , and M918T, M918V, L925I, F1020S and F1538I in para . Copy number variation in ace showed mixed associations with resistance, potentially reflecting the co‐occurrence of variable gene copies and target‐site mutations segregating within and among populations. Finally, we observed putative compositional and structural differences in genomic regions containing carboxylesterases with high ace ‐like homology, a group of genes that might be involved in organophosphate metabolism. This study advances the genomic and molecular resources available for H. destructor , and represents the most comprehensive investigation to date of resistance mechanisms and their spatiotemporal distribution in this invasive pest. Our data showed that pesticide resistance in H. destructor likely involves many genes. Nevertheless, target‐site mutations are likely to remain key markers for rapid resistance diagnostics, for which our KASP markers will provide valuable tools.

New genes and gene functions are key drivers of evolutionary innovation. Venomous animals, such as cone snails, provide striking examples of gene innovation, yet the mechanisms by which toxins arise remain poorly understood. Using the Conus textile genome, we uncover how neuropeptide genes were recruited into the venom and neofunctionalized as doppelgänger toxins. We identify over 20 independent recruitment events that evolved dynamically across the Conus lineage. Rather than arising from ohnologs of a whole-genome duplication event ∼200 mya, these toxins evolved through diverse mechanisms, including exon shuffling, alternative splicing, and ectopic recombination, often facilitated by lineage-specific transposable elements. Our findings reveal a dynamic interplay between genome architecture and molecular innovation, offering broad insight into the evolution of complex gene repertoires in venoms and beyond.

Genomic resources provide tools for understanding the evolution of resistance and monitoring resistance as it develops, which can assist the adoption of pesticide resistance management strategies. The invasive redlegged earth mite, Halotydeus destructor , is a major pest of grain and pasture crops in Australia and is increasingly developing resistance to broad-spectrum pesticides. Here, we assembled a chromosomal-level genome of H. destructor , which comprises eight chromosomes totalling 46 Mb. We also compiled a rich genomic dataset of 190 H. destructor populations (whole-genome pooled sequencing) collected across its invasive Australian range (thousands of kilometers), in four years (2018, 2021, 2022, and 2023), and generated resistance phenotypes to multiple pesticide compounds widely used to manage this pest. These genomic resources were used to provide the most detailed characterisation of genetic structure in Australia to date, highlighting complex patterns of regional structuring and isolation-by-distance. We then screened this population genomic dataset to identify target-site mutations in the ace (acetylcholinesterase) and para (voltage-gated sodium channel) genes, which are the targets of organophosphate and pyrethroid pesticides, respectively. Genotype–phenotype associations suggest that the ace G119S mutation has a strong contribution to chlorpyrifos resistance, but not omethoate resistance. Association tests also suggest that para L1024F mutation has a strong, but weakening, contribution to pyrethroid resistance. We then developed and validated a Kompetitive allele-specific PCR (KASP) assay for the ace G1195S and para L1024F mutations linked to chlorpyrifos and bifenthrin resistance, respectively, and demonstrate how these assays can be applied to quantify allele frequencies in pooled DNA extractions. The KASP markers that we have developed will be valuable in facilitating rapid spatiotemporal screening of key resistance mutations in target genes. Our work also suggests a non-target gene basis for omethoate resistance, and a potential shift to other non-target gene mechanisms for pyrethroid resistance. To that end, our new chromosome-level assembly will be important for characterising the genetic architecture of those resistances.