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McCormick, M.

Publications and source records attributed to McCormick, M..

6 recordsLinked to original sources

Diverse Patterns of Allele-Specific Expression in Healthy Human Tissues

Differences in gene sequence and gene expression underlie variation in traits. However, even monozygotic twins do not express their genes in the same way, develop divergence in traits, and succumb to distinct chronic diseases. During development, epigenetic silencing programs cause diversity in allele expression, resulting in differences in traits and chronic disease risk. To quantify human autosomal allele expression between individuals, we analyzed human allele-specific expression data from the GTEx project. For hundreds of genes, some individuals will express the gene biallelically, while many others may only express one allele or extreme bias towards one allele. We found gene-specific patterns of interindividual variation in allele bias. We found that some individuals have more genome-wide monoallelic/biased expression than others. Individuals also had distinct combinations of allele expression bias. These differences can underlie variation in traits, idiopathic or incompletely penetrant traits/diseases, and chronic diseases. Significance/ImpactAllele-specific expression can affect cancer, immune response, and genetic disease. This work reveals 1) gene-specific multimodal patterns of interindividual variation in allele bias, 2) that individuals can maintain bias across tissues, and 3) that different individuals have distinct combinations of silenced alleles. These different patterns and the weighted classifications demonstrate how allele bias manifests between individuals; there are individuals and tissues with more biased/non-Mendelian expression and some tissues have more age-related changes in which alleles are silenced.

genomics↗

Preserved particulate organic carbon is likely derived from the subsurface sulfidic photic zone of the Proterozoic Ocean: evidence from a modern, oxygen-deficient lake

I-AbstractBiological processes in the Proterozoic Ocean are often inferred from modern oxygen-deficient environments (MODEs) or from stable isotopes in preserved sediment. To-date, few MODE studies have simultaneously quantified carbon fixation genes and attendant stable isotopic signatures. Consequently, how carbon isotope patterns reflect these pathways has not been thoroughly vetted. Addressing this, we profiled planktonic productivity and quantified carbon fixation pathway genes and associated carbon isotope values of size-fractionated (0.2 - 2.7 and > 2.7 m) particulate organic carbon values (813CPOC) from meromictic Fayetteville Green Lake, NY, USA. The high-O2 Calvin-Benson-Bassham (CBB) gene (cbbL) was most abundant in the <2.7 m size fraction in shallow oxic and deep hypoxic waters, corresponding with cyanobacterial populations. The low-O2 CBB gene (cbbM) was most abundant near the lower oxycline boundary in the larger size fraction, coincident with purple sulfur bacteria populations. The reverse citric acid cycle gene (aclB) was equally abundant in both size fractions in the deepest photic zone, coinciding with green sulfur bacteria populations. Methane coenzyme reductase A (mcrA), of anaerobic methane cyclers, was most abundant at the lower oxycline boundary in both size fractions, coinciding with Methanoregula populations. 813CPOC values overlapped with the high-O2 CBB fixation range except for two negative excursions near the lower oxycline boundary, likely reflecting assimilation of isotopically-depleted groundwater-derived inorganic carbon by autotrophs and acetate oxidation by sulfate-reducers. Throughout aphotic waters, 813CPOC values of the large size fraction became 13C-enriched, likely reflecting abundant purple sulfur bacterial aggregates. Microalgal-like isotopic signatures corresponded with increases in cbbL, cbbM and aclB, and enrichment of exopolymer-rich prokaryotic photoautotrophs aggregates. Results suggest that 813CPOC values of preserved sediments from areas of the Proterozoic Ocean with sulfidic photic zones may reflect a mixture of alternate carbon-fixing populations exported from the deep photic zone, challenging the paradigm that sedimentary stable carbon isotope values predominantly reflect oxygenic photosynthesis from surface waters.

microbiology↗

NEUROMETABOLOMIC IMPACTS OF MODELED WILDFIRE SMOKE AND PROTECTIVE BENEFITS OF ANTI-AGING THERAPEUTICS IN AGED FEMALE C57BL/6J MICE

Wildland fires have become progressively more extensive over the past 30 years in the US, and now routinely generate smoke that deteriorates air quality for most of the country. We explored the neurometabolomic impact that smoke derived from biomass has on older (18 months) female C57BL/6J mice, both acutely and after 10 weeks of recovery from exposures. Mice (N=6/group) were exposed to wood smoke (WS) 4 hours/day, every other day, for 2 weeks (7 exposures total) to an average concentration of 0.448mg/m3 per exposure. One group was euthanized 24 hours after the last exposure. Other groups were then placed on 1 of 4 treatment regimens for 10 weeks after wood smoke exposures: vehicle; resveratrol in chow plus nicotinamide mononucleotide in water (RNMN); senolytics via gavage (dasatanib+quercetin; DQ); or both RNMN with DQ (RNDQ). Among the findings, the aging from 18 months to 21 months was associated with the greatest metabolic shift, including changes in nicotinamide metabolism, with WS exposure effects that were relatively modest. WS caused a reduction in NAD+ within the prefrontal cortex immediately after exposure and a long-term reduction in serotonin that persisted for 10 weeks. The serotonin reductions were corroborated by forced swim tests, which revealed an increased immobility (reduction in motivation) immediately post-exposure and persisted for 10 weeks. RNMN had the most beneficial effects after WS exposure, while RNDQ caused markers of brain aging to be upregulated within WS-exposed mice. Findings highlight the persistent neurometabolomic and behavioral effects of woodsmoke exposure in an aged mouse model. Significance StatementNeurological impacts of wildfire smoke are largely underexplored but include neuroinflammation and metabolic changes. The present study highlights modulation of major metabolites in the prefrontal cortex and behavioral consequences in aged (18 month) female mice that persists 10 weeks after wood smoke exposure ended. Supplements derived from the anti-aging field were able to mitigate much of the woodsmoke effect, especially a combination of resveratrol and nicotinamide mononucleotide.

pharmacology and toxicology↗

OME-Zarr: a cloud-optimized bioimaging file format with international community support

A growing community is constructing a next-generation file format (NGFF) for bioimaging to overcome problems of scalability and heterogeneity. Organized by the Open Microscopy Environment (OME), individuals and institutes across diverse modalities facing these problems have designed a format specification process (OME-NGFF) to address these needs. This paper brings together a wide range of those community members to describe the cloud-optimized format itself - OME-Zarr - along with tools and data resources available today to increase FAIR access and remove barriers in the scientific process. The current momentum offers an opportunity to unify a key component of the bioimaging domain -- the file format that underlies so many personal, institutional, and global data management and analysis tasks.

bioinformatics↗

Ancient Yersinia pestis genomes provide no evidence for the origins or spread of the Justinianic Plague

Along with the publication of 137 ancient human genomes retrieved from archaeological remains of the Eurasian steppe, Damgaard et al., 2018 identified two individuals infected with Yersinia pestis, yielding one genome with 0.24x average coverage (DA147, 6th-9th c. AD) and another with 8.7x (DA101, 2nd-3rd c. AD). A phylogenetic analysis performed on the latter placed it in a position ancestral to a 6th-century Justinianic genome from Aschheim, Germany. These results are used to fuel an argument that the Justinianic Plague (541-544 AD) "was brought to Europe towards the end of the Hunnic period through the Silk Road along the southern fringes of the steppes" in contrast to the leading hypothesis of introduction via the Red Sea that is supported by historical accounts. In our reanalysis, we question the contested historical context of the presented genomes with the Justinianic Plague and show that the lower coverage genome might be rather related to the Black Death (1346-1353 AD).

evolutionary biology↗

Ancient Yersinia pestis genomes from across Western Europe reveal early diversification during the First Pandemic (541-750)

The first historically documented pandemic caused by Yersinia pestis started as the Justinianic Plague in 541 within the Roman Empire and continued as the so-called First Pandemic until 750. Although palaeogenomic studies have previously identified the causative agent as Y. pestis, little is known about the bacteriums spread, diversity and genetic history over the course of the pandemic.\n\nTo elucidate the microevolution of the bacterium during this time period, we screened human remains from 20 sites in Austria, Britain, Germany, France and Spain for Y. pestis DNA and reconstructed six new genomes. We present a novel methodological approach assessing SNPs in ancient bacterial genomes, facilitating qualitative analyses of low coverage genomes from a metagenomic background. Phylogenetic analysis reveals the existence of previously undocumented Y. pestis diversity during the 6th-7th centuries, and provides evidence for the presence of multiple distinct Y. pestis strains in Europe. We offer genetic evidence for the presence of the Justinianic Plague in the British Isles, previously only hypothesized from ambiguous documentary accounts, as well as southern France and Spain, and that southern Germany seems to have been affected by at least two distinct Y. pestis strains. Four of the reported strains form a polytomy similar to others seen across the Y. pestis phylogeny, associated with the Second and Third Pandemics. We identified a deletion of a 45 kb genomic region in the most recent First Pandemic strain affecting two virulence factors, intriguingly overlapping with a deletion found in 17th-18th-century genomes of the Second Pandemic.\n\nSignificance StatementThe first historically reported pandemic attributed to Yersinia pestis started with the Justinianic Plague (541-544) and continued for around 200 years as the so-called First Pandemic. To date, only one Y. pestis strain from this pandemic has been reconstructed using ancient DNA. In this study, we present six new genomes from Britain, France, Germany and Spain, demonstrating the geographic range of plague during the First pandemic and showing microdiversity in the Early Medieval Period. Moreover, we detect similar genome decay during the First and Second Pandemic (17th to 18th century) that includes the same two virulence factors, thus providing an example of potential convergent evolution of Y. pestis during large scale epidemics.

evolutionary biology↗