Biology subjects

Turner, E.

Publications and source records attributed to Turner, E..

5 recordsLinked to original sources

bioRxiv2026

Evolution and integration of a novel cell type in the housefly Love Spot

The addition of new neuron types is thought to underlie the evolution of complex nervous systems, yet the mechanisms by which they arise remain unclear. Here we investigate the evolution of a novel target detection photoreceptor in the housefly Musca domestica. In males, a dorso-frontal eye region known as the "Love Spot" enables rapid detection and tracking of females during mating flights. In this region, R7 photoreceptors - normally dedicated to color vision - are repurposed for target detection through altered Rhodopsin expression, physiology, and circuit connectivity. We show that these Love Spot R7 cells (LsR7) are initially specified as canonical R7 photoreceptors but later adopt a chimeric identity combining transcription factors normally associated with either color or motion vision. The sex-determination transcription factor Doublesex (Dsx) is strongly upregulated after R7 specification and, together with the transcription factor Spineless, drives the LsR7 gene regulatory program. Because Dsx upregulation occurs after initial axon targeting to the medulla, LsR7 axons subsequently shorten to connect with lamina neurons and OFF-pathway motion vision circuits. These findings show how new combinations of cell-identity regulators can generate novel neural cell types while revealing developmental constraints imposed by evolutionary history.

Developmental Biology↗

bioRxiv2026

The small RNA Teg16 represses rsbV and modulates SigB-dependent gene expression in Staphylococcus aureus

Staphylococcus aureus relies on coordinated regulatory networks to adapt to environmental stress and host-associated conditions. The alternative sigma factor SigB plays a central role in this process and is controlled by the anti-anti-sigma factor RsbV, which functions as a key regulatory node in the pathway. While numerous small regulatory RNAs (sRNAs) have been identified in S. aureus, relatively few have been directly linked to the SigB stress response network. Here, we investigated the role of the small RNA Teg16 in post-transcriptional regulation of the SigB stress response pathway. Computational prediction identified a region of complementarity between Teg16 and the translational initiation region of rsbV. To test a potential regulatory effect based on this prediction, teg16 was overexpressed, and rsbV transcript levels were measured by quantitative RT-PCR. Teg16 overexpression resulted in reduced rsbV transcript levels and decreased expression of SigB-dependent genes, including asp23 and the carotenoid (crt) biosynthesis operon responsible for staphyloxanthin pigment production. In addition, strains carrying the teg16 expression construct exhibited altered hemolytic activity under the conditions tested, suggesting effects on virulence-associated phenotypes. We further examined whether Teg16 influences the global regulator CodY and observed reduced codY transcript levels at early time points following teg16 overexpression. Together, these results extend a previously identified regulatory relationship between Teg16 and CodY and raise the possibility of a feedback relationship linking post-transcriptional regulation to metabolic control. These findings identify Teg16 as a previously uncharacterized regulator that connects small RNA-mediated control to the SigB stress response network in S. aureus. ImportanceThe alternative sigma factor SigB is a central regulator of stress adaptation in Staphylococcus aureus and influences both metabolism and virulence-associated phenotypes. While numerous small regulatory RNAs (sRNAs) have been identified in this organism, few have been functionally linked to control of the SigB pathway. Here, we identify the small RNA Teg16 as a regulator of rsbV, a key modulator of SigB activity. Teg16-dependent repression of rsbV is associated with reduced expression of SigB-dependent genes and measurable changes in phenotype, including decreased pigment production and altered hemolytic activity. In addition, our findings extend a previously identified relationship between Teg16 and the global regulator CodY, suggesting integration of post-transcriptional regulation with metabolic control. These results establish Teg16 as a previously uncharacterized component of the SigB regulatory network and provide new insight into how small RNAs contribute to stress adaptation in S. aureus.

microbiology↗

bioRxiv2025

Comparative vector competence of post-2015 St. Louis encephalitis virus in Culex tarsalis and Culex quinquefasciatus mosquitoes

The human pathogenic orthoflavivirus St. Louis encephalitis virus (SLEV) reemerged in the western United States in 2015 after more than a decade of absence and has since expanded throughout California with sustained interannual transmission. This shift from the historically sporadic pattern of SLEV activity before 2003 raises the question of whether contemporary strains differ in fitness from earlier strains. To assess whether reemerging SLEV possess enhanced infectivity or transmissibility, we compared five contemporary genotype III strains from California (2016-2023) with a historical genotype V strain from 2003. Growth kinetics were evaluated in mammalian, duck, and mosquito cells; vector competence was assessed in laboratory colonies of Culex tarsalis and Culex quinquefasciatus vectors; and viremia profiles were measured in Collaborative Cross recombinant intercross mice. Some genotype III strains produced higher titers than the historical genotype V strain in avian and mosquito but not mammalian cells. Several genotype III strains infected and transmitted SLEV RNA more efficiently than the historical strain in both mosquito species, although no temporal trend in fitness was observed. SLEV fitness was comparable or greater in Culex quinquefasciatus than in Culex tarsalis. Sequencing identified no shared amino acid substitutions associated with vector infection phenotypes. Although genotype III strains exhibited a delayed peak relative to the historical strain, murine viremia levels were comparable across strains. These findings show some contemporary strains exhibit equal or greater fitness than the historical strain, which may contribute to SLEV persistence and spread in California, underscoring the need for continued surveillance and targeted vector control. IMPORTANCESt. Louis encephalitis virus (SLEV) reemerged in California in 2015 after more than a decade of absence and has since established sustained transmission and expanded geographically. The factors underlying this reemergence remain poorly understood. By comparing contemporary genotype III SLEV strains with a historical genotype V strain, we found that several contemporary strains exhibit equal or greater fitness compared to the historical strain in avian and mosquito cells and are transmitted more efficiently by the two principal California vector species, Cx. tarsalis and Cx. quinquefasciatus. We also demonstrate that Cx. quinquefasciatus can transmit infectious genotype III SLEV, supporting its role in SLEV maintenance and spread. Despite differences in mosquito infection and transmission, we found no evidence that fitness in mosquito vectors or mice has continued to rise among strains detected more recently, suggesting that enhanced transmission is not driven by ongoing directional adaptation. These findings indicate that contemporary genotype III SLEV strains possess transmission competence in mosquito vectors that may have contributed successful reestablishment and persistence of SLEV California. Improved understanding of the characteristics of reemerging SLEV strains can inform surveillance, risk assessment, and vector control efforts aimed at reducing human exposure to prevent disease caused by SLEV.

microbiology↗

bioRxiv2025

Unmasking Pathogen Traits for Chronic Colonization in Neurogenic Bladder Patients

Individuals with neurogenic bladder are particularly susceptible to both chronic bacterial colonization of the bladder and urinary tract infections (UTIs). Neurogenic bladder can arise from a variety of diseases such as diabetes, spinal cord injuries, and spina bifida. To study the ecological and evolutionary dynamics of the microbiome in neurogenic bladder, we developed a longitudinal cohort of 77 children and young adults with spina bifida from two medical centers. We used enhanced urine culture, 16S rRNA sequencing, and whole genome sequencing to characterize the microbial composition of urine and fecal samples. In addition to prospective sample collection, we retrieved prior bacterial isolates from enrolled patients from Vanderbilts clinical microbial biobank, MicroVU. This allowed us to compare bacterial isolates from the same patients over a period of five years. Urine samples were characterized by high abundance of urinary pathogens, such as E. coli and Klebsiella. From longitudinal isolates from individual patients, we identified two common patterns of urinary tract colonization. We observed either the rapid cycling of strains and/or species, often following antibiotic treatment, or we observed the persistence of a single strain across timepoints. Neither persistence of a strain nor colonization with a new strain or species was associated with increased antibiotic resistance. Rather, in paired longitudinally collected strains from the same patients, mutations were identified in genes that code for cell envelope components associated with immune or phage evasion. Experimental testing revealed that O-antigen/LPS biosynthesis mutations confer protection from the immune system while altering susceptibility to phage predation, reflecting a fitness trade-off. We argue that this unparalleled cohort offers the opportunity to identify mechanisms of bacterial adaptation to the urinary tract that can be exploited in future therapeutic approaches.

microbiology↗

bioRxiv2024

foxg1a is required for hair cell development and regeneration in the zebrafish lateral line

Mechanosensory hair cells located in the inner ear mediate the sensations of hearing and balance. If damaged, mammalian inner ear hair cells are unable to regenerate, resulting in permanent sensory deficits. Aquatic vertebrates like zebrafish (Danio rerio) have a specialized class of mechanosensory hair cells found in the lateral line system, allowing them to sense changes in water current. Unlike mammalian inner ear hair cells, lateral line hair cells can robustly regenerate following damage. In mammalian models, the transcription factor Foxg1 functions to promote normal development of the inner ear. Foxg1a is expressed in lateral line sensory organs in zebrafish larvae, but its function during lateral line development and regeneration has not been investigated. We find that loss of Foxg1a function results in reduced hair cell development and regeneration, as well as decreased cellular proliferation in the lateral line system. These data suggest that Foxg1 may be a valuable target for investigation of clinical hair cell regeneration. Summary statementOur work demonstrates a role for Foxg1a in developing and regenerating new sensory cells through proliferation.

developmental biology↗