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Bruckner, A.

Publications and source records attributed to Bruckner, A..

2 recordsLinked to original sources

Evolutionary assembly of cooperating cell types in an animal chemical defense system

A long-standing challenge in biology is explaining how the functions of multicellular organs emerge from the underlying evolution of cell types. We deconstructed evolution of an organ novelty: a rove beetle gland that secretes a defensive cocktail. We show that gland function was pieced together via assembly of two cell types that manufacture distinct compounds. One cell type forms a chemical reservoir in the beetles abdomen and produces alkane and ester compounds. We demonstrate that this cell type is a hybrid of cuticle cells and ancient pheromone and adipocyte-like cells, and executes its function via a mosaic of enzymes sourced from each parental cell type. The second cell type synthesizes noxious benzoquinones using a chimeric pathway derived from conserved cellular energy and cuticle formation pathways. We present evidence that evolution of each cell type was shaped by coevolution between the two cell types: the benzoquinones produced by the second cell type dissolve in solvents produced by the first, yielding a potent secretion that confers adaptive value onto the gland as a whole. Our findings illustrate how cooperation between cell types can arise, generating new, organ-level behaviors.

evolutionary biology↗

Exploring the Stony Coral Tissue Loss Disease Bacterial Pathobiome

A devastating novel coral disease outbreak, referred to as Stony Coral Tissue Loss Disease (SCTLD), was first described in 2014. It is thought to have originated offshore of Miami-Dade County, FL, but has persisted and spread, affecting new reefs along the Florida Reef Tract and reefs of at least 8 other Caribbean jurisdictions. We investigated the microbial communities of clinically normal and diseased specimens of five species of affected corals using targeted 16S ribosomal DNA sequencing (Illumina MiSeq). Fifty-nine bacterial sequences were identified using contrast analysis that had enriched abundance in diseased coral host microbiomes relative to the microbiomes of clinically normal hosts. Several sequences from known bacterial pathogens were identified in this group. Additionally, we identified fifty-three bacterial species that had differentially elevated numbers in clinically normal coral host samples relative to samples from diseased host corals. The bacterial consortia composing the clinically normal and diseased coral microbiomes were clearly distinct taxonomically. Predicted functional profiles based on taxonomy, however, were found to be quite similar. This indicates a high level of functional redundancy among diseased and clinically normal microbiome members. Further examination of the direct sequencing data revealed that while some bacteria were differentially distributed according to disease status, others were not. Fifty-one bacterial species were found in both diseased and clinically normal coral host samples and not differentially abundant in either disease state. These still may be important in explaining the presentation of disease. IMPORTANCEDetermining causation is a management top priority to guide control and intervention strategies for the SCTLD outbreak. Towards this goal we examined bacterial taxa that were differentially elevated in numbers in diseased corals as compared to clinically normal corals at Looe Key, FL in August 2018. Many of the bacterial species we detected are known to be pathogenic to humans, animals, and (or) plants, and some of these have been found associated with diseased corals in other studies. Microbes that were present (or conspicuous by their absence) in both diseased as well as clinically normal corals were also examined because "healthy" corals from a diseased location such as Looe Key may have been exposed but may not have been showing overt disease at the time of sampling. Although untangling of causation is not possible currently, certain bacterial cliques and excess nutrients appear to be potential risk factors in SCTLD pathology.

microbiology↗