Drift in small populations predicts mate availability and the breakdown of self-incompatibility in a clonal polyploid.

Mate limitation in small populations can reduce reproductive fitness, hinder population growth, and increase extinction risk. Mate limitation is exacerbated in self-incompatible (SI) taxa, where shared S-alleles further restrict mating. Theory suggests genetic drift as a predictor of mate limitation and the breakdown of SI systems.

Melioidosis in goats at a single Australian farm was caused by multiple diverse lineages of Burkholderia pseudomallei present in soil.

Background: Burkholderia pseudomallei, causative agent of melioidosis, is a One Health concern as it is acquired directly from soil and water and causes disease in humans and agricultural and wild animals. We examined B. pseudomallei in soil and goats at a single farm in the Northern Territory of Australia where >30 goats acquired melioidosis over nine years.

Analysis of mitochondrial protein translocation by disulfide bond formation and cysteine specific crosslinking.

Protein translocation is a highly dynamic process and, in addition, mitochondrial protein import is especially complicated as the majority of nuclear encoded precursor proteins must engage with multiple translocases before they are assembled in the correct mitochondrial subcompartment. In this chapter, we describe assays for engineered disulfide bond formation and cysteine specific crosslinking to analyze the rearrangement of translocase subunits or to probe protein-protein interactions between precursor proteins and translocase subunits. Such assays were used to characterize the translocase of the outer membrane, the presequence translocase of the inner membrane and the sorting and assembly machinery for the biogenesis of β-Barrel proteins.

Restriction of innate Tγδ17 cell plasticity by an AP-1 regulatory axis.

IL-17-producing γδ T (Tγδ17) cells are innate-like mediators of intestinal barrier immunity. While Th17 cell and ILC3 plasticity have been extensively studied, the mechanisms governing Tγδ17 cell effector flexibility remain undefined. Here, we combined type 3 fate-mapping with single cell ATAC/RNA-seq multiome profiling to define the cellular features and regulatory networks underlying Tγδ17 cell plasticity.