Biology subjects

Gheorghe, I.

Publications and source records attributed to Gheorghe, I..

3 recordsLinked to original sources

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↗

bioRxiv2022

Ultra-sensitive coupling between organ growth and size by YAP-1 ensures uniform body plan proportions in C. elegans

Imbalance between the growth rate of different organs can amplify to large deviations of their size proportions during development. We show that, for the C. elegans pharynx, such size divergence is prevented by reciprocal coordination of pharyngeal growth with other tissues. Live imaging of hundreds of individuals revealed that small pharynxes grow more rapidly than large pharynxes, catching up in volume during development. Moreover, pharynx-to-body size proportions were robust to even strong tissue-specific inhibition of mTORC1 and insulin signalling. Tissue-specific depletion of these pathways slowed-down the growth of the respective tissue and additionally triggered a systemic growth response that ensured appropriate organ size proportions. By mathematical modelling, we show that the conservation of proportions requires a bi-directional ultra-sensitive coupling of body growth and pharynx size that cannot be explained by a reduction of food uptake alone. Instead, organ growth coordination requires regulation by the mechano-transducing transcriptional co-activator YAP/yap-1. Knock-down of yap-1 makes animals sensitive to tissue-specific inhibition mTORC1 inhibition, causing a disproportionate pharynx and developmental arrest. Our data suggests that mechano-transduction tightly coordinates organ growth during C. elegans development to ensure the uniformity of body plan proportions among individuals.

developmental biology↗