bioRxiv Science⌕ Search

bioRxiv · 10.1101/2025.09.23.678041

The livebearers platyfish and swordtails partially regenerate their hearts with persistent scarring

Abstract

Heart regeneration varies among vertebrates, with zebrafish serving as a reference species for efficient cardiac restoration. How this capacity diversified across teleosts is an emerging question, particularly following the recent identification of non-regenerative cardiac repair in medaka and cavefish. Here, we investigate heart restorative capacity following cryoinjury in two livebearers, platyfish and swordtails (Xiphophorus species), belonging to the Poeciliidae family. We demonstrate that their hearts lack the vascularized compact myocardium, a ventricular layer implicated in the restorative response in zebrafish. Following cryoinjury, both poeciliids failed to rapidly deposit fibrotic tissue that normally reinforces the damaged ventricle. This deficiency correlates with pronounced wound protrusion. Although the remaining myocardium displayed an initial proliferative response, subsequently deposited collagenous scar tissue permanently sealed the ventricular wall, precluding complete regeneration. Transcriptomic analysis identified several divergently regulated pathways between cryoinjured hearts of zebrafish and platyfish, most notably in immune response regulation. These differences were validated by delayed leukocyte infiltration and sustained inflammation in platyfish, contrasting with the rapid and self-resolving inflammatory response in zebrafish. Our findings demonstrate that Xiphophorus species have evolved hearts with compromised regenerative capacity, characterized by initial wound protrusion and permanent scarring. These results establish that lineage-specific evolutionary traits can profoundly shape regenerative competence across teleosts, with broad implications for understanding the mechanistic basis of cardiac repair. Highlights{middle dot} Viviparous poeciliids lack vascularized compact myocardium. {middle dot} Inflammation and fibrosis are delayed in the cryoinjured platyfish ventricle. {middle dot} Ventricular cryoinjury in Xiphophorus leads to transient bulging-type deformation. {middle dot} Failure to form a myocardial bridge results in permanent scarring.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Hisler, V., Rees, L., Blanchoud, S., Lischer, H. E. L., Bruggmann, R., Jazwinska, A.. 2025-09-25. The livebearers platyfish and swordtails partially regenerate their hearts with persistent scarring. https://doi.org/10.1101/2025.09.23.678041

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Proteome-wide quantification of protein turnover in frog and fly embryos reveals divergent strategies of maternal inheritance

Every embryo inherits a maternal proteome that it must remodel with zygotic proteins to build its many cell types. The fate of the maternal proteome remains contested because indirect measurements cannot resolve it. Here, we combine 18O-water labeling with multiplexed proteomics to quantify protein turnover proteome-wide in frog and fly embryos. Through hatching, the frog preserves the bulk of its maternal proteome, confining rapid degradation to a small regulatory module. The fly cannot meet its synthesis demand from yolk alone and instead degrades nearly all maternal proteins, including housekeeping proteins long assumed stable, recycling them into new protein. Yet the turnover hierarchy is conserved, with disordered and regulatory proteins degrading fastest, while the fly rescales the whole proteome ~eightfold faster. These results recast the developmental proteome as both informational inheritance and metabolic reserve, establish 18O-water labeling as a turnover method for non-feeding organisms, and provide a resource of embryonic half-lives.

developmental biology↗

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↗

Network topology reveals distinct forms of developmental leverage in the Drosophila wing

Developmental gene regulatory networks reliably transform positional information into complex multicellular form, yet the organizational principles linking network architecture to developmental mechanism remain poorly understood. Here, we analyzed the Drosophila melanogaster wing developmental network to determine whether network topology reflects the distribution of developmental leverage during organogenesis. Integration of curated wing-development genes with high-confidence STRING interactions revealed five Hierarchical Layers of Developmental Control (HLDCs) associated with distinct topological and developmental roles. Organizer Centers, Signaling Scaffolds, and Pattern Implementers formed a forward-specification axis in which connectivity progressively contracted as positional information was transformed into increasingly localized developmental programs. Interface Coordinators departed from this hierarchy through disproportionate brokerage, whereas Local Modulators retained connectivity despite localized developmental scope. We propose that these complementary signatures reflect two regulatory architectures: 1) hierarchical information propagation that generates developmental identity and 2) distributed homeostatic regulation that coordinates and refines developmental outputs. Within Character Identity Modules (ChiMOs), this architecture links conserved patterning systems, Hox-defined contexts, and organ-specific kernels to reproducible morphology, providing a mechanistic hypothesis for developmental canalization and experimentally testable predictions.

developmental biology↗