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Schroeder, N.

Publications and source records attributed to Schroeder, N..

5 recordsLinked to original sources

Coexistence of phasmid sensory neurons and caudal glands offers a new perspective on cell type evolution in nematodes

The highly conserved body plan of nematodes makes members of this phylum excellent models to study cell type evolution. Early branching nematode lineages, mostly occupying aquatic habitats, usually contain caudal glands deployed for underwater attachment to a substrate, but have been thought to lack phasmid sensory organs, resulting in their historical classification as "Aphasmidia". With the transition to a terrestrial environment, nematodes lost caudal glands and gained phasmid sensory neurons. The supposed mutually exclusive existence of caudal glands and phasmids has led to the suggestion that phasmid neurons may have evolved from caudal glands. Here, we rule out this possibility through light and electron microscopical analysis of Mononchus aquaticus, a member of the early branching Dorylaimia lineage, showing that phasmid sensory neurons and caudal glands do coexist. This observation not only argues against a proposed cell type evolution scenario accompanying aquatic-to-terrestrial transitions but also indicates that the presence of phasmid sensory organs may have been an ancestral trait of the nematode phylum.

evolutionary biology↗

Analysis of Nematode Ventral Nerve Cords Suggests Multiple Instances of Evolutionary Addition and Loss of Neurons

Despite their diversity in habitats, nematodes are often considered to have a highly conserved neuroanatomy. This premise is based on only a subset of the nematode phylogenetic tree focused on the more diverged clades within the class Chromadorea, which includes the model organism Caenorhabditis elegans, thereby limiting our understanding of macroevolutionary trends in nervous system structure. To approach this problem, we used nuclear morphology to quantify the number of neurons in the nematode ventral nerve cord (VNC) to identify evolutionary patterns in neuroanatomical organization within the basal clades of Chromadorea and Enoplea. DAPI staining revealed significant VNC neuron count variations among families, with notable differences between the classes Enoplea and Chromadorea and among Enoplean species. These results may indicate a degree of evolutionary morphological stasis in later diverging Chromadorean clades. To further examine developmental patterns and potential variation in Enoplean nervous system architecture, we established an isogenic culture of the nematode Mononchus aquaticus. We found that while M. aquaticus contained four times as many VNC neuronal nuclei as C. elegans, the VNC had a similar developmental timeline during post-embryonic stages. However, dye-filling assays revealed an extensive distribution of neurons along the lateral body wall, which have no obvious homolog to C. elegans. We found that M. aquaticus is capable of sustained movement following bisection that may imply a more distributed nervous system network. Our results provide a roadmap for understanding phylum-wide nervous system evolution and demonstrate large-scale differences between Enoplean and Chromodorean nervous systems.

evolutionary biology↗

Characterization of muscle growth and sarcomere branching in the striated musculature of C. elegans.

Muscle structure is dynamically shaped by mechanical use, yet how distinct locomotor behaviors influence sarcomere organization remains poorly understood. In Caenorhabditis elegans, crawling and swimming constitute discrete gaits that differ in curvature, frequency, and mechanical load, providing a tractable model for studying activity-dependent remodeling. Using confocal imaging of phalloidin-stained body-wall myocytes, we quantified myocyte geometry, sarcomere length, and sarcomere number across anterior, medial, and posterior regions in animals reared exclusively under crawling or swimming conditions. Quantification and hypothesis testing used linear mixed models that accounted for repeated myocyte measurements within animals, with interaction terms testing region-specific effects of locomotor condition after IQR-based outlier removal. Swimming produced characteristic remodeling of body-wall muscles. Myocytes elongated globally, while selectively thinning in the mid-body, reducing cell area by [~]13 % relative to crawlers. Shape metrics confirmed this shift: circularity declined at mid- and tail-regions and anisotropy increased by [~]2-3 units. Sarcomere architecture exhibited parallel remodeling. Average sarcomere length shortened across the body (-0.19 {micro}m in head, -0.35 {micro}m in mid-body, -0.20 {micro}m in tail), while sarcomere number increased anteriorly and medially (+0.77 and +0.65 sarcomeres per myocyte). The medial region also showed a significant rise in sarcomere density, indicating tighter serial packing. These adaptations mirror functional compartmentalization predicted from gait kinematics and parallel fast-fiber remodeling observed in vertebrate muscles. The results indicate that C. elegans muscles adapt their contractile lattice to sustained mechanical demand, linking neural gait selection and mechanosensitive signaling to long-term structural plasticity. This work establishes C. elegans as a model for dissecting the conserved pathways that couple muscle use to cellular architecture and provides a foundation for future comparisons of healthy and diseased muscle remodeling. Short summaryMuscle cells in C. elegans change their structure according to how the animals move. Worms that swim develop shorter, more densely packed sarcomeres and elongated body-wall muscles, while crawlers maintain longer, broader fibers. These adaptations enhance flexibility and power transmission for high-frequency motion, linking neural gait selection and mechanosensitive signaling to long-term remodeling of the contractile lattice.

molecular biology↗

Atoh8 acts as a regulator of chondrocyte proliferation and differentiation in endochondral bones

Atonal homolog 8 (Atoh8) is a transcription factor of the basic helix-loop-helix (bHLH) protein family, which is expressed in the cartilaginous elements of endochondral bones. To analyze its function during chondrogenesis we deleted Atoh8 in mice using a chondrocyte- (Atoh8flox/flox;Col2a1-Cre) and a germline- (Atoh8flox/flox;Prx1-Crefemale) specific Cre allele. In both strains, Atoh8 deletion leads to a reduced skeletal size of the axial and appendicular bones, but the stages of phenotypic manifestations differ. While we observed obviously shortened bones in Atoh8flox/flox;Col2a1-Cre mice only postnatally, the bones of Atoh8flox/flox;Prx1-Crefemale mice are characterized by a reduced bone length already at prenatal stages. Detailed histological and molecular investigations revealed reduced zones of proliferating and hypertrophic chondrocytes. In addition, Atoh8 deletion identified Atoh8 as a positive regulator of chondrocyte proliferation. As increased Atoh8 expression is found in the region of prehypertrophic chondrocytes where the expression of Ihh, a main regulator of chondrocyte proliferation and differentiation, is induced, we investigated a potential interaction of Atoh8 function and Ihh signaling. By activating Ihh signaling with Purmorphamine we demonstrate that Atoh8 regulates chondrocyte proliferation in parallel or downstream of Ihh signaling while it acts on the onset of hypertrophy upstream of Ihh likely by modulating Ihh expression levels.

developmental biology↗

The nidogen-domain containing protein DEX-1 is required for epidermal remodeling in C. elegans dauers

Phenotypic plasticity is a critical component of an organisms ability to thrive in an ever-changing environment. The free-living nematode, Caenorhabditis elegans, adapts to unfavorable environmental conditions by pausing reproductive development and entering a stress-resistant larval stage known as dauer. The transition into dauer is marked by vast morphological changes - including remodeling of epidermis, neurons and muscle. Though many of these dauer-specific traits have been described, the molecular basis of dauer-specific remodeling is still poorly understood. Here we show that the nidogen-domain containing protein DEX-1 functions downstream of the dauer decision to facilitate stage-specific tissue remodeling during dauer morphogenesis. DEX-1 was previously shown to regulate sensory dendrite formation during embryogenesis. We find that DEX-1 is also required for the proper remodeling of the stem cell-like epidermal seam cells and maintenance of seam cell quiescence during dauer. dex-1 mutant dauers lack distinct lateral cuticular alae during dauer and have increased sensitivity to sodium dodecyl sulfate (SDS). Furthermore, we find that DEX-1 mediated seam cell remodeling is required for proper dauer mobility. We show that DEX-1 acts cell autonomously in the seam cells during dauer and that dex-1 expression during dauer is regulated through DAF-16/FOXO-mediated derepression. Finally, we show that dex-1 interacts with a family of zona pellucida-domain encoding genes to regulate dauer-specific epidermal remodeling. Taken together, our data indicates that DEX-1 plays a central role in C. elegans epidermal remodeling during dauer.

genetics↗