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Biology subjects

Conklin, E.

Publications and source records attributed to Conklin, E..

3 recordsLinked to original sources

Comparative connectomics of parasite esophagus suggests evolutionary simplification of a nervous system

Several prominent examples suggest that the evolution of parasitism is accompanied by nervous system simplification. However, it is unclear if this is a generalizable rule and whether parasite- associated simplification occurs at the level of synaptic connectivity. The nematode esophagus is a specialized neuromuscular feeding organ that varies with diet and lifestyle. Plant-parasitic nematodes are major agricultural pests that feed through a protrusible stylet and release of extensive glandular effectors; however, the neuronal mechanisms controlling parasite feeding are unclear. Here, we used serial-section electron microscopy to reconstruct the esophageal connectome of the infective second-stage juvenile of the soybean cyst nematode, Heterodera glycines, and compared it with those of the free-living species Caenorhabditis elegans and Pristionchus pacificus. Similar to these species, H. glycines has 20 esophageal neurons with relatively conserved cell body positions. Despite this conservation, the H. glycines chemical synaptic network is highly reduced in output to musculature. A unique ensheathment of neurons by a gland cell facilitates novel synaptic connectivity in H. glycines. The H. glycines esophageal network is strongly biased toward monadic synapses and shows a greater proportion of neuron- neuron and neuron-gland connections. Consistent with a reduction in motor output, network analysis indicates that the H. glycines esophageal network is smaller and less clustered than free-living species. Using centrality analysis and synthetic ablation, we predict that control of multiple feeding modules in H. glycines depends on distinct neurons compared to free-living species. These findings show how parasitism reshapes a feeding circuit and identify candidate species-specific circuits for parasite control. Significance statementAnimal nervous systems are tuned to the behaviors they support. Nematodes occupy diverse ecological niches, and their feeding organ, the esophagus, is specialized to their diet. Understanding the esophageal nervous system provides evolutionary insights into parasitism as well as pathways for future control targets. We present the esophageal connectome of the soybean cyst nematode Heterodera glycines, which causes devastating damage to soybean production worldwide. By comparing H. glycines and free-living species, which diverged over 350 million years ago, we identify evolutionarily conserved features of the feeding circuit and highlight parasite-specific circuits as candidate targets for control.

neuroscience↗

Regulatory architecture controlling terminal differentiation of an interoceptive paraneuron in C. elegans

Interoceptive paraneurons are neuron-like cells located within internal epithelial cell surfaces that sense internal stimuli to evoke specific behavioral or physiological responses. The elucidation of terminal differentiation programs of paraneurons is expected to provide insights into how epithelial cells acquire neuron-like feature during development and possibly also over evolutionary time. We define here transcriptional programs that control the terminal differentiation of an interoceptive paraneuron class in the nematode C. elegans, called uv1. The uv1 cells sense mechanosensory inputs in the uterus and signal via the HSN neurons to modulate egg-laying behavior. We show that like in canonical neurons, the neuron-like secretory features of uv1 are controlled by a combination of CUT homeobox genes, while the combinatorial terminal gene battery that defines the unique functional features of uv1 is jointly controlled by a combination of at least three transcription factors, a LIM homeodomain (LIN-11), a SoxD (EGL-13) and a Pax family (EGL-38) protein. These factors act in a terminal selector-type manner to jointly co-regulate the many distinct uv1-paraneuron specific molecular features, such as sensory receptors, neuromodulatory receptors and neuropeptides, as well as uv1s tyraminergic identity. Our findings demonstrate notable similarities in the dichotomous architecture of gene regulatory programs of neurons and paraneurons.

developmental 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↗