Search bioRxiv⌕ Search

bioRxiv · 10.1101/2024.02.14.580276

Duplication of the anteroposterior body axis in postembryos of the Eratigena atrica spider

Abstract

Many factors, including temperature, can affect the embryonic development of spiders, leading to a variety of deformities in their body structure. Early studies on teratological changes in spiders were aimed mainly at describing the morphology of affected individuals. Now, with new tools and molecular techniques used to carry out a functional analysis of genes involved in body segmentation and leg formation, the explanation of these defects is finally possible. In our new experiment on spiders collected in 2022/2023 breeding season, we obtained 87 postembryos with various body defects by applying alternating temperatures (140C and 320C) for the first 10 days of embryonic development. The most common anomaly, i.e. oligomely, occurred in 70 individuals, while other defects (schistomely, symely, polymely, heterosymely) were noted sporadically. Partial prosoma duplication affected only six embryos. In the context of recent advances in molecular spider embryology we conclude that recorded anomalies may be connected with the suppression or erroneous expression of certain genes of body segmentation and appendage formation, and by disturbances in the formation and migration of the cumulus, which leads to an axis duplication phenotype. Summary statementThis article presents a rare anomaly - bicephaly, which appeared in spider postembryos as a result of thermal shocks applied during embryogenesis.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Napiorkowska, T., Templin, J., Napiorkowski, P.. 2024-02-14. Duplication of the anteroposterior body axis in postembryos of the Eratigena atrica spider. https://doi.org/10.1101/2024.02.14.580276

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↗