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Biology subjects

Hatch, A. J.

Publications and source records attributed to Hatch, A. J..

2 recordsLinked to original sources

Global untreated wastewater hosts a vast reservoir of previously uncharacterized microbial lineages

Untreated wastewater are reservoirs of microbial communities originating from different sources within an urbanized human-populated area and is now regularly used for tracking and assessing levels of certain human pathogens like SARS-CoV-2, Salmonella, and Poliomyelitis. Wastewater microbial communities can exhibit high diversity, comprised of mostly non-pathogens alongside a smaller population of pathogens. Much of the research on wastewater has focused on either pathogens or microbiomes in the treatment plants, but not on the microbiome of untreated wastewater, which is perhaps more reflective of community health. Moreover, as wastewater usage expands to more known and unknown pathogen detection, a deeper understanding of both wastewaters overall genetic diversity and diversity over time is pivotal. Towards that goal, we characterized the observed microbial diversity of global untreated wastewater by analyzing 1,344 publicly available metagenomes, representing 6 continents, and created a global wastewater database hosted at https://doi.org/10.5281/zenodo.17794790. We elucidated the full spectrum of prokaryotic diversity by recovering and characterizing high quality bins, contigs, and reads from all the data. We provide the first comprehensive, publicly available database describing global wastewater by uncovering previously uncharacterized microbes, identifying geographically specific microbial populations, and creating a high-quality dataset to advance future microbiome, epidemiological, and biosurveillance research.

genomics↗

Tafazzin regulates the function of lipopolysaccharide activated B lymphocytes in mice

B lymphocytes are responsible for humoral immunity and play a key role in the immune response. Optimal mitochondrial function is required to support B cell activity during activation. We examined how deficiency of tafazzin, a cardiolipin remodeling enzyme required for mitochondrial function, alters the metabolic activity of B cells and their response to activation by lipopolysaccharide in mice. B cells were isolated from 3 month old wild type or tafazzin knockdown mice and incubated for up to 72 h with lipopolysaccharide and cell proliferation, expression of cell surface markers, secretion of antibodies and chemokines, proteasome and immunoproteasome activities, and metabolic function determined. In addition, proteomic analysis was performed to identify altered levels of proteins involved in survival, immunogenic, proteasomal and mitochondrial processes. Compared to wild type lipopolysaccharide activated B cells, lipopolysaccharide activated tafazzin knockdown B cells exhibited significantly reduced proliferation, lowered expression of cluster of differentiation 86 and cluster of differentiation 69 surface markers, reduced secretion of immunoglobulin M antibody, reduced secretion of keratinocytes-derived chemokine and macrophage-inflammatory protein-2, reduced proteasome and immunoproteasome activities, and reduced mitochondrial respiration and glycolysis. Proteomic analysis revealed significant alterations in key protein targets that regulate cell survival, immunogenicity, proteasomal processing and mitochondrial function consistent with the findings of the above functional studies. The results indicate that the cardiolipin transacylase enzyme tafazzin plays a key role in regulating mouse B cell function and metabolic activity during activation.

immunology↗