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Wayhs, B.

Publications and source records attributed to Wayhs, B..

2 recordsLinked to original sources

Evolving Threats: Leveraging C. elegans to Decode the Virulence Profiles of Highly Related Environmental Salmonella Newport Isolates

Salmonella enterica subspecies enterica, particularly serovar Newport, remains a leading cause of foodborne illnesses in the United States, implicated in numerous outbreaks associated with a diverse array of food products. This study rigorously investigates the virulence of five distinct S. Newport isolates, characterized by varying patterns of pulse-field gel electrophoresis (PFGE) molecular-diagnostic subtyping, using the nematode Caenorhabditis elegans as a host model organism. We conducted viability assays on C. elegans to evaluate how these isolates affect nematode survival. The selected bacterial strains, rooted in historical foodborne outbreak significance but environmentally isolated, were previously sequenced to provide a comprehensive genomic framework. A notable focus of our research was on the nearly genetically identical PFGE types Newport-61 and the Newport-1015 isolates, which differ by a [~]1.7 Mb genomic inversion. C. elegans survival assays in response to pathogenic-strain infections revealed that one Newport-1015 and the Newport-61 were particularly more virulent compared to other strains tested. These findings enhance our understanding of the pathogenic potential of environmental S. Newport and highlight the need to understand the regulatory mechanisms that contribute to virulence capacity.

microbiology↗

LIPL-1 and LIPL-2 are TCER-1-regulated Lysosomal Lipases with Distinct Roles in Immunity and Fertility

Reproduction and immunity are fundamental, energy intensive processes that often compete for resources, leading to trade-offs observed across diverse species. Lipid metabolism plays a crucial role in integrating these processes, particularly during stressful conditions such as pathogenic infections. Yet the molecular mechanisms governing this integration remain poorly understood. TCER-1, the C. elegans homolog of mammalian TCERG1, suppresses immunity and promotes fertility, especially upon maternal infection. Here, we show that TCER-1 regulates two conserved lysosomal lipases, lipl-1 and lipl-2, to balance reproduction, immunity and lifespan. Using transcriptomic, lipidomic, and molecular-genetic analyses, we demonstrate that while both lipl-1 and lipl-2 mediate infection-induced lipid remodeling, lipl-1 enhances immunity and catalyzes the accumulation of ceramide species linked to stress response and longevity, whereas, lipl-2 unexpectedly does not. Both lipases contribute towards fertility outcomes, but lipl-2 is especially critical for maintaining embryonic-eggshell integrity during maternal infection and aging. Strikingly, expression of human lysosomal acid lipase (LAL), the ortholog of lipl genes, rescues the immune defects triggered by lipl-l loss and enhances immune resilience. Together, these findings uncover functionally distinct roles for lipl-1 and lipl-2 in modulating lipid species that shape immune fitness, healthspan and reproductive health, and suggest a potentially conserved mechanism by which lipid metabolism links fertility and immunity.

genetics↗