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Bartley, A.

Publications and source records attributed to Bartley, A..

2 recordsLinked to original sources

Experimental evolution of symbiotic microbes without their partners can imply the presence of cooperative or antagonistic adaptations

Microbes adapt to the presence of other species, but the fitness consequences of specific interactions are difficult to study in their natural context. We experimentally evolved symbiotic microbes in an artificial environment without access to the partners with whom they interact in nature. As organisms will tend to lose adaptations that they do not need due to drift or pleiotropic tradeoffs, we expect normally symbiotic microbes evolved in isolation to lose adaptations to help or harm their natural partners. The direction and magnitude of such changes can suggest whether the microbes had historically been selected to help or harm one another. We apply this method to the symbiosis between the social amoeba Dictyostelium discoideum and three intracellular bacterial endosymbionts, Paraburkholderia agricolaris, P. hayleyella, and P. bonniea. A minority of strains of Paraburkholderia and D. discoideum evolved differences in their effects on one anothers fitnesses, implying the existence of adaptations to one another that were lost when no longer relevant. Our results suggest that the degree to which D. discoideum and Paraburkholderia have adapted to help or harm one another can differ substantially between strains within each species, with some strains appearing to have a historically adversarial relationship, some strains a more benign relationship, and many strains no clear adaptations to one another at all. Our results underscore the complexity of microbial interactions in nature and suggest experimental evolution under relaxed selection is a potentially useful approach for studying adaptation in microbes.

evolutionary biology↗

Ectopically Expressed Rhodopsin Is Not Sensitive to X-rays

Visual perception of X-radiation is a well-documented, but poorly understood phenomenon. Early literature implicates scotopic rod cells and rod opsin in X-ray detection, however, evidence suggests that X-rays excite the retina via a different mechanism than visible light. While rhodopsins role in X-ray perception is unclear, the possibility that it could function as an X-ray receptor has led to speculation that it could act as a transgenically expressed X-ray receptor. If so, it could be used to transduce transcranial X-ray signals and control the activity of genetically targeted populations of neurons in a less invasive version of optogenetics, X-genetics. Here we investigate whether human rhodopsin (hRho) is capable of transducing X-ray signals when expressed outside of the retinal environment. We use a live-cell cAMP GloSensor luminescence assay to measure cAMP decreases in hRho-expressing HEK293 cells in response to visible light and X-ray stimulation. We show that cAMP GloSensor luminescence decreases are not observed in hRho-expressing HEK293 cells in response to X-ray stimulation, despite the presence of robust responses to visible light. Additionally, irradiation had no significant effect on cAMP GloSensor responses to subsequent visible light stimulation. These results indicate that ectopically expressed rhodopsin does not function as an X-ray receptor, and suggest that it is not capable of transducing transcranial X-ray signals into neural activity for X-ray mediated, genetically targeted neuromodulation.

neuroscience↗