Biology subjects

Psalmon, S.

Publications and source records attributed to Psalmon, S..

6 recordsLinked to original sources

bioRxiv2026

ALIGN: A modular framework for quantitative analysis of longitudinal development in Caenorhabditis elegans

Longitudinal live imaging is a powerful tool for studying growth, development and behaviour. However, reproducible and scalable analysis of the large resulting datasets remains a major bottleneck. Here, we present ALIGN (Automated Longitudinal Image-based Growth aNalyzer), a modular framework that integrates deep learning-based segmentation, automated quality control, computational straightening, feature extraction and interactive annotation within a single configurable pipeline that can be operated end-to-end by users without coding expertise. Applying ALIGN to longitudinal development of C. elegans, we demonstrate accurate segmentation across heterogeneous imaging conditions, detection of larval stage transitions from growth trajectories, and data-driven quality control, ensuring high measurement precision. Computational straightening and alignment enable consistent analysis of motile animals, removing motion artefacts from three-dimensional optical sectioning. Applying ALIGN to measure pharyngeal pumping and growth rates in wild-type and eat-2 mutants uncovered a non-proportional relationship between feeding and growth. ALIGN thus provides generalizable tools and resources for longitudinal, single-animal analysis of development.

developmental biology↗

bioRxiv2026

Temporal compression of gonadal growth preserves reproductive timing and soma-to-germline scaling under stress

How organisms maintain timely reproduction under stress is central to life history plasticity and remains an unmet challenge in biomedicine. Life history theory predicts that organisms preserve fitness across environments by reallocating resources between somatic and reproductive growth, yet direct tests of this prediction have been limited by the lack of longitudinal life history data. Here, using Caenorhabditis elegans, we combine longitudinal video microscopy of gonadal growth, mathematical modelling, and genetic perturbations to show that reproductive timing is preserved through temporally dynamic control of reproductive organ growth. Under stress, the onset of gonad growth was delayed early in development but later accelerated relative to somatic growth, thereby preserving reproductive-to-somatic size ratios at adulthood. Modelling suggests this delay-and-acceleration strategy to minimize the time to maturity under stress. Consistently, disrupting compensatory gonadal growth acceleration, either through genetic perturbation of the JNK/p38 stress signalling pathway or by uncoupling of reproductive and somatic development, reduced gonad size and delayed reproduction. Together, our results show that reproductive robustness under stress arises from dynamic regulation of reproductive growth rather than a fixed shift in resource allocation, defining a previously unrecognized mechanistic principle for environmentally plastic sexual maturation.

developmental biology↗

bioRxiv2026

The MAPK phosphatase VHP-1 buffers pharynx-to-body proportions against tissue-specific growth imbalance in C. elegans

Maintaining appropriate organ size ratios in the face of growth fluctuations is critical for the development of a reproducible body plan. Yet the mechanisms involved remain poorly understood. Here, we investigated how pharynx-to-body proportions are maintained in Caenorhabditis elegans, combining tissue-specific perturbations, genetic screening, and longitudinal live imaging. A genome-wide RNAi screen revealed that knock-down of the dual-specificity MAPK phosphatase VHP-1 turns animals hypersensitive to inter-tissue growth imbalance caused by pharyngeal or epidermal depletion of the mTORC1 activator RAGA-1 or the ribosomal protein RPL-22. In contrast, vhp-1 mutants tolerated global raga-1 loss, indicating a specific requirement for vhp-1 under tissue growth imbalance. Knock-down of the p38 pathway suppressed the imbalance-specific defects of vhp-1 mutants. In contrast, JNK knock-down effectively rescued the pleiotropic phenotypes of vhp-1 mutants but only weakly reduced their sensitivity to RAGA-1 imbalance, indicating that these two stress-MAPK pathways make distinct contributions to the response to growth imbalance. Finally, whole-animal VHP-1 levels increased upon epidermal RAGA-1 depletion, and epidermal VHP-1 depletion did not reproduce the sensitivity caused by global vhp-1 loss, consistent with a contribution from VHP-1 outside the growth-perturbed epidermis in buffering against local growth imbalance.

developmental biology↗

bioRxiv2025

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↗

bioRxiv2024

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↗

bioRxiv2023

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↗