Biology subjects

Mathias, N.

Publications and source records attributed to Mathias, N..

3 recordsLinked to original sources

bioRxiv2025

Canopy1/Cnpy1 is required for proper V2R processing and transport; its loss impairs the function and circuit organization of basal/V2R vomeronasal sensory neurons

The vomeronasal organ (VNO) is a specialized chemosensory structure in the nasal cavity that detects pheromones and mediates social and reproductive behaviors. The VNO of rodents is populated by different types of vomeronasal sensory neurons (VSNs). Apical VSNs, located near the lumen, express the transcription factor (TF) Meis2, V1R family receptors, and the G protein subunit Gao; the VSNs distributed closer to the basal lamina express the TF Tfap2e/AP-2{varepsilon}, V2R receptors, and the G protein subunit Gai2. In addition, sparse cells in the VNO express the Formyl Peptide Receptors (FPRs). Single-cell mRNA sequencing (scRNA Seq) identified over 980 differentially expressed genes between these cell types, with many linked to the endoplasmic reticulum (ER). Among these ER proteins, Canopy1 (Cnpy1), was found to be among the most enriched genes in V2R+ VSNs. Previously studied only in zebrafish, Cnpy1 was found to affect Fgfr1 signaling and is thus also known as "FGF signaling regulator-1". In a previous study, we discovered that AP-2e upregulates Cnpy1 expression. Although Cnpy1 knockout mice are viable and have normal VNO development at birth, they experience a progressive degeneration and loss of V2R-expressing VSNs. Prior to symptoms, the basal VSNs of KO mice display reduced V2R protein immunoreactivity in the soma and a complete absence of the protein at the lumen of the VNO, rendering the neurons non-functional. Cnpy1 KOs exhibit altered guidance cues and adhesion molecule expression, along with disrupted connectivity to the accessory olfactory bulb (AOB). Our study shows that distinct neuronal types depend on unique ER protein repertoires to maintain proper proteostasis. The loss of Cnpy1 highlights the importance of cell-type-specific ER factors in the differentiation and function of specific neurons, revealing mechanisms that drive neuronal diversity and vulnerability to ER gene disruption.

neuroscience↗

bioRxiv2019

Increased temperatures reduce the vectorial capacity of Aedes mosquitoes for Zika virus

Rapid and significant range expansion of both ZIKV and its Aedes host species has resulted in ZIKV being declared a global health threat. Mean temperatures are projected to increase globally, likely resulting in alterations of the transmission potential of mosquito-borne pathogens. The relationship between temperature and ZIKV transmission has not been well characterised for Aedes aegypti and Aedes albopictus.\n\nTo understand the effect of diurnal temperature range on the vectorial capacity of Aedes aegypti and Aedes albopictus for ZIKV, factors contributing to transmission potential were measured at different temperature regimens. Their longevity and blood feeding rates were assessed, and vector competence was determined following feeding on blood meals with 8.3 log10 PFU/ml ZIKV.\n\nHigher temperature resulted in decreased longevity of Ae. aegypti [Log-rank (Mantel-Cox) Test, Chi-square, df 35.66, 5 P (<0.0001)] and a significant decrease in blood feeding rates across groups [Z score (-5.8478) P (0.0444)]. Temperature had a population and species-specific impact on ZIKV infection rates. Overall, Ae. albopictus reared at the lowest temperature regimen demonstrated the highest vectorial capacity (1.63) and the highest transmission efficiency (57%). Temperature increases decreased vectorial capacity across groups, yet the largest decreases were measured for Ae. aegypti.\n\nThe results of this study suggest that future climate change could significantly impact vector competence, blood feeding behavior and longevity, and therefore decrease the overall vectorial capacity of Aedes mosquitoes. It is also clear that this impact is likely to be both species and population-specific.

microbiology↗

bioRxiv2019

Zika virus infection and temperature significantly impact Aedes albopictus gut microbiota

Elizabethkingia anophelis has been the cause of four outbreaks with significant morbidity and mortality. Its transmission routes remain unknown and no point source of infection has been identified. Here we show that E. anophelis can be found in the saliva of Aedes mosquitoes, suggesting the novel possibility of vector-borne transmission of this bacterium. We additionally characterized diverse microbial communities in Aedes midguts, salivary glands and saliva. To the best of our knowledge, this represents the first description of the microbiome of Aedes saliva. Further, we demonstrate that increased abundance of E. anophelis is associated with decreased susceptibility and replication of Zika virus (ZIKV) in the midgut of Aedes mosquitoes, suggesting a novel transmission barrier for arboviruses transmitted by Aedes mosquitoes. Together, these results demonstrate the complex relationships between the mosquito, the midgut microbial community and arboviruses and offer insights into the epidemiology and control of emerging bacterial and viral pathogens. Author SummaryElizabethkingia anophelis has in the recent past caused outbreaks different parts of the world resulting both in morbidity and mortality. Until now, to the best of our knowledge, no study has been able to demonstrate that this bacterium can be transmitted by mosquitoes. We have demonstrated for the first time that Elizabethkingia anophelis is present in the saliva of both infected and non-infected Aedes mosquitoes. Further, we have shown that it confers an inhibitory effect on Zika virus establishment in the midguts of Aedes mosquitoes. Together, these results potentially display the potential for vector borne transmission of E. anophelis as well as a novel transmission barrier of ZIKV. Lastly, we have for the first time characterized salivary microbes of Aedes mosquitoes necessitating the investigation of the impact of salivary microbes in severity of disease in vertebrate hosts.

microbiology↗