Comparative genomics and genome-wide SNPs of endangered Eld's deer provide breeder selection for inbreeding avoidance.

Eld's deer, a conserved wildlife species of Thailand, is facing inbreeding depression, particularly in the captive Siamese Eld's deer (SED) subspecies. In this study, we constructed genomes of a male SED and a male Burmese Eld's deer (BED), and used genome-wide single nucleotide polymorphisms to evaluate the genetic purity and the inbreeding status of 35 SED and 49 BED with limited pedigree information. The results show that these subspecies diverged approximately 1.26 million years ago. All SED were found to be purebred. A low proportion of admixed SED genetic material was observed in some BED individuals. Six potential breeders from male SED with no genetic relation to any female SED and three purebred male BED with no relation to more than 10 purebred female BED were identified. This study provides valuable insights about Eld's deer populations and appropriate breeder selection in efforts to repopulate this endangered species while avoiding inbreeding.

Pseudomonas aeruginosa adapts to octenidine via a combination of efflux and membrane remodelling.

Pseudomonas aeruginosa is an opportunistic pathogen capable of stably adapting to the antiseptic octenidine by an unknown mechanism. Here we characterise this adaptation, both in the laboratory and a simulated clinical setting, and identify a novel antiseptic resistance mechanism. In both settings, 2 to 4-fold increase in octenidine tolerance was associated with stable mutations and a specific 12 base pair deletion in a putative Tet-repressor family gene (smvR), associated with a constitutive increase in expression of the Major Facilitator Superfamily (MFS) efflux pump SmvA. Adaptation to higher octenidine concentrations led to additional stable mutations, most frequently in phosphatidylserine synthase pssA and occasionally in phosphatidylglycerophosphate synthase pgsA genes, resulting in octenidine tolerance 16- to 256-fold higher than parental strains. Metabolic changes were consistent with mitigation of oxidative stress and altered plasma membrane composition and order. Mutations in SmvAR and phospholipid synthases enable higher level, synergistic tolerance of octenidine.