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Biology subjects

Meyer, A. R.

Publications and source records attributed to Meyer, A. R..

7 recordsLinked to original sources

Lichen symbiosis does not impose a uniform genomic syndrome on algae

Symbiosis has lasting effects on the genomic evolution of interacting organisms. Shifting niches and selection intensities are well-documented drivers of adaptive evolution, but nonadaptive evolution is an equally important, if less conspicuous, dimension of symbiont genome evolution. Through a reduction in effective population size (Ne), symbiosis can reduce the efficacy of natural selection in symbionts; however, evidence of this "genomic syndrome" is derived almost entirely from bacteria. Whether it extends to eukaryotic symbioses with complex demography remains unclear. Here, lichen-forming algae are examined for signatures of a genome-wide reduction in the efficacy of selection arising from demographic shifts associated with symbiosis. To test this, four lichen-forming algal taxa were compared to their closest free-living relatives using complementary measures of (i) the strength of molecular evolution (dN/dS, K), (ii) codon use bias (ENC), and (iii) base composition at synonymous sites (GC3). Lichen-forming algae showed heterogeneous responses across all signatures of molecular evolution examined. The effect of lifestyle (lichen-forming vs. free-living) on dN/dS ratios and codon use bias was lineage specific. GC3 was uniformly reduced in lichen-forming taxa, but the underlying causes differed, and no genes showed uniformly intensified or relaxed selection across all four lichen-forming taxa. These results suggest that, while symbiosis often reshapes symbiont population genetics in ways that elevate the role of drift, lichen-forming algae do not show a uniform reduction in the efficacy of selection. Rather, the demographic effects and functional demands of each specific lichen symbiosis likely shape genome evolution in lineage-specific ways.

evolutionary biology↗

Environmental conditions drive selection and recovery following disease-induced declines

Emerging infectious diseases threaten public health and biodiversity across the globe1,2. Disease outcomes are frequently dependent on local environmental conditions3-5, but how these factors shape host adaptation and long-term recovery are often unknown6. Here we combine two decades of population, disease, and environmental data with a common garden experiment to investigate the drivers of variable declines and recovery for remnant bat populations following the emergence of the fungal disease, white-nose syndrome. We find that initial declines were greater and faster in warmer sites (88.3% vs. 74.2% in cold sites), but these populations recovered more quickly and hosts developed higher resistance (1.5x reduction of fungal loads) than populations from colder sites that were buffered from initial impacts. Our experimental data suggest that warm sites served as hotspots of host adaptation where selective pressures were stronger because thermal conditions approached optimal growth for the pathogen, which eventually favored the development of high pathogen resistance. Populations in colder sites experienced weaker selective pressure and thus remain more susceptible, although bats from larger colonies were more likely to survive, suggesting that adaptive traits exist in these populations, but at much lower frequency. These findings show that the environmental conditions that initially buffer populations from collapse can simultaneously constrain their evolutionary response to emerging threats, and ultimately determine differential recovery following disease-induced declines.

ecology↗

Virus-like antigen display delivers a stand-alone danger signal through the BCR that circumvents tolerance

How B cells discriminate self from foreign antigens remains a central question, given inherent autoreactivity of the mature B cell receptor (BCR) repertoire. Soluble antigen (sAg) induces tolerance, whereas patterned antigen display on virus-like particles (pAg) triggers robust B cell responses that can proceed without T cell help. Here, we show how this divergence arises early in BCR signaling. Unlike sAg, pAg can bypass a Lyn-dependent negative feedback loop to trigger digital signaling, such that ultra-low concentrations of pAg produce strong and sustained Ca2+ responses. Surprisingly, pAg drives maximal nuclear NF-{kappa}B but limited NFAT, whereas sAg does the opposite, reflecting differential production of diacylglycerol. Consequently, sAg induced an NFAT-dependent anergy program, whereas pAg evaded this state and instead engaged a cMyc-driven program that partially resembles a TLR-dependent danger response. Our findings reveal how proximal signaling directs distinct transcriptional fate to enable immunogenic B cell responses to virus-like antigen display.

immunology↗

Shipped and shifted: modeling collection-induced bias in microbiome multi-omics using a tractable fermentation system

Large-scale, decentralized microbiome sampling surveys and citizen science initiatives often require periods of storage at ambient temperature, potentially altering sample composition during collection and transport. We developed a generalizable framework to quantify and model these biases using sourdough as a tractable fermentation system, with samples subjected to controlled storage conditions (4 {degrees}C, 17 {degrees}C, 30 {degrees}C, regularly sampled up to 28 days). Machine-learning models paired with multi-omics profiling -- including microbiome, targeted and untargeted metabolome profiling, and cultivation -- revealed temperature-dependent shifts in bacterial community structure and metabolic profiles, while fungal communities remained stable. Storage induced ecological restructuring, marked by reduced network modularity and increased centrality of dominant taxa at higher temperatures. Notably, storage duration and temperature were strongly encoded in the multi-omics data, with temperature exerting a more pronounced influence than time. 24 of the top 25 predictors of storage condition were metabolites, underscoring functional layers as both sensitive to and informative of environmental exposure. These findings demonstrate that even short-term ambient storage (< 2 days) can substantially reshape microbiome, metabolome, and biochemical profiles, posing risks to data comparability in decentralized studies and emphasizing the need to recognize and address such biases. Critically, the high predictability of storage history offers a path toward bias detection and correction -- particularly when standardized collection protocols are infeasible, as is common in decentralized sampling contexts. Our approach enables robust quantification and modeling of such storage effects across multi-omics datasets, unlocking more accurate interpretation of large-scale microbiome surveys.

microbiology↗

Rising together: Exploring Sourdough Fermentation Diversity through Co-design in the HealthFerm Citizen Science Initiative

Fermented foods are culturally significant and increasingly recognized for their potential health benefits, yet scientific data on household fermentation practices remain limited. We launched a co-designed citizen science (CS) initiative within the HealthFerm project to collect sourdough fermentation data across Europe. Over 1000 participants from 33 countries registered, with 671 samples submitted, enabling large-scale analysis of fermentation practices, motivations, and sourdough characteristics. Participants also completed standardized at-home experiments and sensory evaluations, generating a dataset linking baking habits with physicochemical and sensory profiles. Distinct patterns emerged: professional bakers used older, more frequently refreshed starters and fermented at higher temperatures. Ingredient choices and motivations varied by country, shaped by perceived health benefits. Beyond data collection, this initiative established a microbial biobank and harmonized metadata resource, while offering practical insights into co- design, logistics, and public engagement. The resulting framework provides a transferable model for participatory research in microbiology and food systems science.

scientific communication and education↗

An integrated signaling threshold initiates IgG response towards virus-like immunogens

Class-switched neutralizing antibody (nAb) production is rapidly induced upon many viral infections. However, due to the presence of multiple components in typical virions, the precise biochemical and biophysical signals from viral infections that initiate nAb responses remain inadequately defined. Using a reductionist system of synthetic virus-like structures (SVLS) containing minimal, highly purified biochemical components commonly found in enveloped viruses, here we show that a foreign protein on a virion-sized liposome can serve as a stand-alone danger signal to initiate class-switched nAb responses in the absence of cognate T cell help or Toll-like receptor signaling but requires CD19, the antigen (Ag) coreceptor on B cells. Introduction of internal nucleic acids (iNAs) obviates the need for CD19, lowers the epitope density (ED) required to elicit the Ab response and transforms these structures into highly potent immunogens that rival conventional virus-like particles in their ability to elicit strong Ag-specific IgG. As early as day 5 after immunization, structures harbouring iNAs and decorated with just a few molecules of surface Ag at doses as low as 100 ng induced all IgG subclasses of Ab known in mice and reproduced the IgG2a/2c restriction that has been long observed in live viral infections. These findings reveal a shared mechanism for nAb response upon viral infection. High ED is capable but not necessary for driving Ab secretion in vivo. Instead, even a few molecules of surface Ag, when combined with nucleic acids within these structures, can trigger strong antiviral IgG production. As a result, the signaling threshold for the induction of neutralizing IgG is set by dual signals originating from both ED on the surface and the presence of iNAs within viral particulate immunogens. One-sentence summaryReconstitution of minimal viral signals necessary to initiate antiviral IgG

immunology↗

Mechanisms of neutralizing antibody response probed using synthetic virus-like structures

The durability of an antibody (Ab) response is highly important for antiviral vaccines. However, due to the complex compositions of natural virions, the molecular determinants of Ab durability from viral infection or inactivated viral vaccines have been incompletely understood. Here we used a reductionist system of liposome-based virus-like structures to examine the durability of Abs in primary immune responses in mice. This system allowed us to independently vary fundamental viral attributes and to do so without additional adjuvants to model natural viruses. We show that a single injection of antigens (Ags) orderly displayed on a virion-sized liposome is sufficient to induce a long-lived neutralizing Ab (nAb) response. Introduction of internal nucleic acids dramatically modulates the magnitude of long-term Ab responses without alteration of the long-term kinetic trends. These Abs are characterized by exceptionally slow off-rates of [~]0.0005 s-1, which emerged as early as day 5 after injection and these off-rates are comparable to that of affinity-matured monoclonal Abs. A single injection of these structures at doses as low as 100 ng led to lifelong nAb production in BALB/c mice. Thus, a minimal virus-like immunogen can give rise to potent and long-lasting antiviral Abs in a primary response in mice without live infection. This has important implications for understanding both live viral infection and for optimized vaccine design.

immunology↗