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Doubleday, P. F.

Publications and source records attributed to Doubleday, P. F..

3 recordsLinked to original sources

Negative and neutral interactions are prevalent in interactions between marine chitin degraders

Bacterial chitin degradation contributes to global carbon cycling, particularly in marine environments where it is a highly abundant polysaccharide. Despite the taxonomic diversity of co-occurring chitin-degrading bacteria, the influence of individual traits on interactions between them remains poorly understood. Here, we measured key physiological traits of seven chitin degraders and investigated how these traits shape interaction outcomes and chitin degradation in pairwise cocultures. We found mainly negative and neutral interactions among degraders, contrasting with the synergistic dynamics observed with other complex polysaccharides. However, chitin degradation was not consistently diminished. These interaction types could be attributed to the limited partitioning of degradation products, alongside variations in enzyme repertoires and attachment behaviours that help some degraders to prevail over others. Further, we showed that one degrader can strongly inhibit the growth of others, even those possessing favourable physiological traits, likely due to the secretion of inhibitory compounds. These findings extend our understanding of the breadth of interactions among primary polysaccharide degraders and their implications for the degradation process. One-sentence SummaryThe physiological traits of bacteria that degrade chitin, a highly abundant biopolymer in marine environments, promote a range of neutral and negative interactions among them.

microbiology↗

Multi-omics analysis of endothelial cells reveals the metabolic diversity that underlies endothelial cell functions

Endothelial cells (ECs) line the vascular system and are key players in vascular homeostasis, yet their metabolic diversity across tissues, vascular beds, and growth states remains poorly understood. This study examines metabolic differences between proliferating and quiescent ECs and compares blood and lymphatic endothelium using proteomics and metabolomics. Our findings indicate that metabolism in quiescent ECs is not dormant but reorganized in a cell-specific manner, with decreased heme intermediates in human umbilical vein ECs and increased branched-chain amino acid catabolism across all quiescent ECs. Consistent with the differences identified in the omics data, perturbation studies revealed that inhibiting enzymes involved in heme, glutamate, fatty acid, and nucleotide biosynthesis led to distinct phenotypic responses in blood and lymphatic ECs. These findings highlight the importance of metabolic pathways in sustaining both proliferating and quiescent ECs and reveal how ECs from different vascular beds rely on distinct metabolic processes to maintain their functional states.

systems biology↗

Dynamic metabolome profiling uncovers potential TOR signaling genes

Although the genetic code of the yeast Saccharomyces cerevisiae was sequenced 25 years ago, the characterization of the roles of genes within it is far from complete. The lack of a complete mapping of functions to genes hampers systematic understanding of the biology of the cell. The advent of high-throughput metabolomics offers a unique approach to uncovering gene function with an attractive combination of cost, robustness, and breadth of applicability. Here we used flow-injection time-of-flight mass spectrometry (FIA-MS) to dynamically profile the metabolome of 164 loss-of-function mutants in TOR and receptor or receptor-like genes under a time-course of rapamycin treatment, generating a dataset with over 7,000 metabolomics measurements. In order to provide a resource to the broader community, those data are made available for browsing through an interactive data visualization app hosted at https://rapamycin-yeast-metabolome.herokuapp.com/. We demonstrate that dynamic metabolite responses to rapamycin are more informative than steady state responses when recovering known regulators of TOR signaling, as well as identifying new ones. Deletion of a subset of the novel genes causes phenotypes and proteome responses to rapamycin that further implicate them in TOR signaling. We found that one of these genes, CFF1, was connected to the regulation of pyrimidine biosynthesis through URA10. These results demonstrate the efficacy of the approach for flagging novel potential TOR signaling-related genes and highlights the utility of dynamic perturbations when using functional metabolomics to deliver biological insight.

systems biology↗