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Psalmon, S.

Publications and source records attributed to Psalmon, S..

3 recordsLinked to original sources

Teach your microscope how to print: Low-cost and rapid-iteration microfabrication for biology

The application of traditional microfabrication techniques to biological research is hindered by their reliance on clean rooms, expensive or toxic materials, and slow iteration cycles. We present an accessible microfabrication workflow that addresses these challenges by integrating consumer 3D printing techniques and repurposing standard fluorescence microscopes equipped with DMDs for maskless photolithography. Our method achieves micrometer-scale precision across centimeter-sized areas without clean room infrastructure, using affordable and readily available consumables. We demonstrate the versatility of this approach through four biological applications: inducing cytoskeletal protrusions via 1 m-resolution surface topographies; micropatterning to standardize cell and tissue morphology; fabricating multilayer microfluidic devices for confined cell migration studies; imprinting agar chambers for long-time tracking of C. elegans. Our protocol drastically reduces material costs compared to conventional methods and enables design-to-device turnaround within a day. By leveraging open-source microscope control software and existing lab equipment, our workflow lowers the entry barrier to micro-fabrication, enabling labs to prototype custom solutions for diverse experimental needs while maintaining compatibility with soft lithography and downstream biological assays.

cell biology↗

Selective autophagy of ribosomes balances a tradeoff between starvation survival and growth resumption

Animals facing fluctuating food availability must balance survival during starvation with rapid resumption of growth when encountering food. We investigated how proteome turnover and remodelling through autophagy influences this trade-off in C. elegans L1 larvae by combining live imaging and proteomics. Starvation triggered an autophagy-dependent, disproportionate loss of ribosomal and other growth-related proteins. Residual ribosomal protein abundance at the end of starvation predicted the rate of growth recovery of individual animals during post-starvation feeding, linking proteome-scale changes to organism-scale life-history. Hyperactivation of the mTORC1 regulator RAGA-1 preserved ribosomal proteins, accelerated recovery after short starvation, but reduced survival under prolonged starvation. These findings identify autophagy-dependent ribosomal protein decline as a central component of starvation-induced proteome remodelling and reveal its role in balancing the trade-off between starvation endurance and recovery speed in a multicellular animal.

physiology↗

Learning accelerates the evolution of slow aging but obstructs negligible senescence

BackgroundFor most animals, intrinsic senescence-induced mortality increases with age, while deaths from extrinsic threats, such as predation or accidents, decline during development as individuals grow and mature. Age-dependent modulation of extrinsic mortality is known to influence the evolution of aging, yet how the timing of mortality shapes evolutionary forces remains poorly understood. ResultsTo address this, we developed two complementary mathematical models that integrate survival benefits arising during development with the progressive increase in mortality associated with senescence. Agent-based simulations and deterministic analyses revealed a strong and consistent influence of the timing of developmental survival benefits on their evolutionary impact: early-life survival benefits reduced the selection for slower aging, while late-acting benefits enhanced it. This difference arises because early-life benefits more strongly accelerate population growth than late-life benefits, diminishing the relative evolutionary advantage of increased longevity. ConclusionsOur results underscore the importance of mortality timing in the evolution of aging and provide a theoretical framework for connecting developmental trajectories to aging dynamics.

evolutionary biology↗