Biology subjects

Neves, F.

Publications and source records attributed to Neves, F..

3 recordsLinked to original sources

bioRxiv2026

BOWIe: Wireless Headstage for Optical Stimulation in Closed-Loop Optogenetics Experiments in Freely-moving Rodents

Optogenetics is an invaluable technique in neuroscience to study brain circuits, but conventional optogenetic systems use tethered approaches to deliver light to the brain which can hinder natural behavior. Optoelectronic advances led to the development of wireless optical stimulators for optogenetics experiments, but most reported devices have low widespread use due to complex builds and reduced versatility, which has also limited their integration in closed-loop systems. Here, we developed BOWIe, a battery-powered, low-weight, wireless headstage for photostimulation in optogenetics experiments with rodents, especially designed for simple integration in multiple behavioral setups, including those requiring closed-loop operation. BOWIe is based on a Bluetooth-Low Energy system-on-a-chip that allows simultaneous control and communication capabilities with a reduced number of components, and can be paired with an Arduino-based transmitter for simple integration in any behavioral paradigm using analogue or digital triggers. Two modes of optical stimulation are possible, either with ferrule-coupled optical fibers or LED neural probes, which permit adapting the headstage according to material availability or experimental demands. A user-friendly app was also developed to simplify headstage pairing, definition of stimulation parameters, and protocol design. BOWIe was validated in two behavioral paradigms, including in a closed-loop experiment using computer vision, Bonsai RX, and Deeplabcut Live to track behavioral parameters online and remotely trigger photostimulation upon detected events. BOWIe's modular design and flexible integration with behavioral setups make it a practical tool for in vivo experiments with optogenetics.

bioengineering↗

bioRxiv2026

Cartilaginous fish inform the lineage-specific evolution and MHC association of the TLR family

Chondrichthyans (sharks, rays and chimaeras) diverged from other vertebrate lineages over 400 million years ago and possess fully functional innate and adaptive immune systems. They comprise over 1,200 species occupying diverse aquatic habitats, from fresh to marine waters and from shallow to deep seas. Exposure to diverse pathogens through time, together with contemporary ocean warming and habitat degradation driven by climate change, has likely shaped unique immune mechanisms in these species. Toll-like receptors (TLRs) are central components of innate immunity, recognizing conserved pathogen-associated molecular patterns and initiating immune responses, yet their diversity remains poorly characterized in Chondrichthyans. Here, we characterize the TLR gene repertoire in elasmobranchs (sharks and rays) using genomic and transcriptomic data. We identify orthologs spanning all known vertebrate TLR families, including genes shared with agnathans as well as gnathostome-specific genes, and detect lineage-specific patterns of TLR duplication and loss, particularly in squaliform sharks and rays. Molecular evolution analyses indicate that most elasmobranch TLRs are under strong purifying selection, with positively selected sites in all genes, consistent with ongoing adaptation to pathogen-and environment-driven pressures. Several TLRs co-localize with genomic regions enriched in immune genes, including MHC paralogous regions, suggesting an ancestral genomic hotspot for vertebrate immunity.

evolutionary biology↗

bioRxiv2021

Convergent loss of the necroptosis pathway in disparate mammalian lineages shapes virus countermeasures

Programmed cell death is a vital process in the life cycle of an organism. Necroptosis, an evolutionary restricted form of programmed necrosis, contributes to the innate immune response by killing pathogen-infected cells. This virus-host interaction pathway is organized around two key components: the receptor-interacting protein kinase 3 (RIPK3), which recruits and phosphorylates the mixed lineage kinase-like protein (MLKL), thus inducing cellular plasma membrane rupture and cell death. Critically, the presence of necroptotic inhibitors in viral genomes validates necroptosis as an important host defense mechanism. Here, we show, counterintuitively, that in different mammalian lineages of mammalian, central components of the necroptotic pathway, such as RIPK3 and MLKL genes, are deleted or display inactivating mutations. Frameshifts or premature stop codons are observed in all the studied species of cetaceans and leporids. In carnivores genomes, the MLKL gene is deleted, while in a small number of species from afrotheria and rodentia premature stop codons are observed in RIPK3 and/or MLKL. Interestingly, we also found a strong correlation between the disruption of necroptosis in leporids and cetaceans and the absence of the C-terminal domain of E3-like homologs (responsible for necroptosis inhibition) in their naturally infecting poxviruses. Overall, our study provides the first comprehensive picture of the molecular evolution of necroptosis in mammals. The loss of necroptosis multiple times during mammalian evolution highlights the importance of gene/pathway loss for species adaptation and suggests that necroptosis is not required for normal mammalian development. Moreover, this study highlights a co-evolutionary relationship between poxviruses and their hosts, emphasizing the role of host adaptation in shaping virus evolution.

evolutionary biology↗