Collinson, D. | Search bioRxiv

bioRxiv2025

Detecting Mitochondrial Free Radicals with Quantum Sensors: From Organelles to a D. melanogaster Model of Neurodegeneration

This study identifies a distinct free radical signature in a D. melanogaster model of Parkinsons Disease, successfully differentiating Pink1-deficient flies from wild-type controls. This insight was achieved using a robust quantum sensing methodology for the selective detection of free radicals in biological systems. Our approach utilizes optically detected magnetic resonance (ODMR) and magnetic modulation (MM) protocols with nanodiamond nitrogen-vacancy (NV) centres. Selective identification is achieved using the spin probe TEMPOL, a cell-permeable superoxide dismutase 2 (SOD2) mimic that initially quenches the photoluminescence signal. Upon scavenging free radicals like hydroxyl and superoxide, TEMPOL is converted to a diamagnetic adduct, restoring the contrast and thus enabling quantitative detection. The approach was first validated in a chemical system with radical generation confirmed by electron paramagnetic resonance (EPR) spectroscopy. It was then demonstrated across biological scales, from isolated mitochondria and whole glioblastoma cells to the Drosophila model. In these studies, high-resolution respirometry revealed distinct free radical signatures, and findings were compared with NV T1 relaxometry. This work provides new biophysical insight into mitochondrial dysfunction, demonstrating a distinct free radical signature in a neurodegeneration model and connecting it to specific metabolic states.

cell biology↗

bioRxiv2025

Symbiotic entrenchment through ecological Catch-22

Symbiotic organisms frequently evolve obligate dependencies on hosts, but the evolutionary changes that entrench such lifestyles are poorly understood. Ant societies are vulnerable to parasitic "myrmecophiles": impostor species that infiltrate colonies and are often unable to survive outside of them. Here we show that obligate dependence of a myrmecophile on its host arises from irreversibility of the fundamental steps that achieve social acceptance inside the nest. We report a convergent system in which parallel rove beetle lineages (Staphylinidae) evolved from free-living ancestors to parasitize the same host ant. Exploiting this system, we uncover cellular mechanisms by which these beetles mimic host ant cuticular hydrocarbons (CHCs): nestmate recognition pheromones, which function pleiotropically to prevent desiccation. We present evidence of a biological stealth mechanism in a rove beetle in which the CHC biosynthetic machinery becomes transcriptionally silenced on entering the nest. Silencing transforms the beetle into a chemical blank slate onto which ant CHCs are horizontally transferred via interspecies grooming behavior. This strategy leads to identical chemical resemblance and seamless social integration within the colony. CHC pathway silencing is irreversible, however, forcing the beetle into a chronic, physically close dependence on ants to both maintain nestmate status and prevent desiccation. Loss of CHC silencing renders the beetle detectable to ants; conversely, loss of behavioral attraction to ants renders the beetle desiccation prone. Our findings show how symbiotic entrenchment can arise from a Catch-22-like ratchet operating at the organismal level.

evolutionary biology↗