Biology subjects

Masters, J.

Publications and source records attributed to Masters, J..

4 recordsLinked to original sources

bioRxiv2026

How to stand out to a mate - Flash colour of Photinus fireflies maximizes signal contrast against ambient light

During twilight, flying male Photinus fireflies flash in search for conspecific females, which sit on the vegetation below and flash back in response. However, before darkness sets in, the green vegetation in the habitat makes the detection of flashes more difficult. Twilight active fireflies tend to emit more yellow flashes than nocturnal fireflies and it has been proposed that firefly flash colour evolved to enhance the contrast of firefly flashes against their signalling background. There is indirect evidence for this contrast hypothesis, but it remains to be rigorously tested. This is the first study to directly test the contrast hypothesis by recording ambient light spectra in three different habitats throughout the daily flash activity of Photinus pyralis and P. australis and comparing these ambient light spectra to the male flash spectra of the two species. The contrast hypothesis predicts that during peak activity, firefly light colour will maximally contrast with the signalling background. Our data show that male flash spectra fit into a gap in the ambient light spectrum that opens during peak flashing activity of each species, effectively enhancing the visual contrast between male flashes and their background and making males more visible to their potential mates.

evolutionary biology↗

bioRxiv2026

A consortium of human commensals protects against middle ear colonization by otopathogens

A year-long sequencing analysis of bacterial commensals sampled from infants during periods in which they were healthy or suffering recurrent ear infections [otitis media (OM)] identified several species of bacterial commensals that correlate with health and absence of ear infections. Here we consider and test the possibility of a causal relationship between a group of commensals and periods of health. We assemble a set of five health-associated bacterial species into a nasopharyngeal commensal consortium (NPCC) and test whether these organisms can effectively colonize the respiratory tracts of mice so that their effects on invading pathogens could be evaluated. We observed that NPCC efficiently colonize mice and that they provide substantial protection against the otopathogens, Streptococcus pneumoniae and Bordetella pertussis, reducing numbers of each in the middle ears by 99 to 99.9%. The NPCC also affected colonization/growth of these pathogens within the lower respiratory tract, suggesting complexity in these interactions. Together these data demonstrate a profound effect of commensals on invading otopathogens and describe a powerful experimental system in which the important interactions between the healthy infant microbiota and invading pathogens can be studied mechanistically.

microbiology↗

bioRxiv2025

Adult mice with neonatal-like T cell subsets exhibit increased susceptibility to Bordetella pertussis and influenza infection

Infants are significantly more susceptible to respiratory infection, often resulting in increased morbidity and hospitalization, and occasionally death. This susceptibility is partially explained by the developing nature of the thymus in human infants at, and for several months after, birth. However, the contribution of T cells produced in this thymic microenvironment to infant immune responses has received minimal investigation. Here, we utilized a previously described mouse model (Foxn1{Delta}/{Delta}) which exhibits a persistently immature thymus. Through further characterization, we have determined that adult Foxn1{Delta}/{Delta} mice retain some unique T cells observed in neonatal mice including CD8{beta}+ {gamma}{delta} T cells and CD8 T cells displaying a memory-like phenotype. For this reason, we assessed the potential of these neonatal-like T responses to two pathogens which disproportionately affect neonates, Bordetella pertussis (Bp) and influenza. Utilizing these infections, we demonstrate that T cells generated in an incompletely developed thymus fail to control or mount an effective response against Bp. We also observe that Foxn1{Delta}/{Delta} mice control acute influenza infection, a response which does not require IL-17. However, the Foxn1{Delta}/{Delta} mice fail to generate an influenza nucleoprotein (NP) specific CD8+ T cell response which is likely associated with their inability to fully clear the infection. Together, these data suggest that Foxn1{Delta}/{Delta} mice can be utilized to study the generation, function, and persistence of some unique T cells made in a neonatal-like thymus.

immunology↗

bioRxiv2020

Plexin-B1 mutation drives prostate cancer metastasis

Prostate cancer mortality is associated with the metastatic spread of tumour cells. A better understanding of the mechanisms which allow a locally advanced tumour to disseminate around the body will identify new therapeutic targets to block this process. One of set of genes implicated in metastasis are plexins, which can promote or suppress tumour progression depending on cancer type and cellular context. We have taken a mouse genetics approach to gain insight into the role of Plexin-B1 in prostate cancer progression in vivo. We show here that genetic deletion of Plexin-B1 in PbCre+Ptenfl/flKrasG12V and PbCre+Ptenfl/flp53fl/fl mouse prostate cancer models significantly decreased metastasis. High levels of prostate epithelial cell-specific expression of wild-type Plexin-B1 in knock-in mice with a PbCre+Ptenfl/flKrasG12V background also significantly decreased metastasis. In contrast, expression of a Plexin-B1 mutant (P1597L; identified from metastatic deposits in prostate cancer patients) in prostate epithelial cells in PbCre+Ptenfl/flKrasG12V and PbCre+Ptenfl/flp53fl/fl mice significantly increased metastasis, in particular metastasis to distant sites. In line with these findings, both deletion and overexpression of wild-type Plexin-B1 reduced invasion of tumour cells into the prostate stroma, while overexpression of mutant Plexin-B1 significantly increased invasion, suggesting that Plexin-B1 has a role in the initial stages of metastasis. Invasion and metastasis also correlated with phosphorylation of myosin light chain, suggesting that Plexin-B1 signals via the Rho/ROCK pathway to promote metastasis. Our results demonstrate that mutant Plexin-B1 promotes metastasis in prostate cancer and represents a new therapeutic target to suppress tumour spread.

cancer biology↗