Biology subjects

Schroeder, N. E.

Publications and source records attributed to Schroeder, N. E..

5 recordsLinked to original sources

bioRxiv2026

High-Resolution Melting (HRM) Assay for Molecular Detection of Calonectria ilicicola in Soybean

Calonectria ilicicola, an emerging and economically important soilborne pathogen in the U.S. Midwest, causes red crown rot (RCR) disease of soybean. It is essential to have an early and accurate detection method for effective management of RCR, since disease symptoms are nearly identical to those of other soybean diseases. In this study, we developed and validated a high resolution melting (HRM) assay targeting the translation elongation factor 1&alpha (TEF-1&alpha) gene for the specific detection of C. ilicicola. The assay was evaluated using a specificity panel of 78 DNA samples, including 67 fungal and oomycete DNA samples and 11 soybean host-DNA samples, as well as DNA from 56 field-collected symptomatic and asymptomatic soybean tissues. The HRM assay generated distinct melting profiles and, where applicable, absence or delayed amplification that reliably differentiated C. ilicicola from non target fungi and oomycetes. Additionally, the marker distinguished three haplotypes among C. ilicicola isolates, consistent with nucleotide polymorphisms in the TEF-1&alpha target region. The assay demonstrated strong quantitative performance, exhibiting high linearity (R^2= 0.9992) and acceptable amplification efficiency (94.05%) across a broad DNA concentration range. In field samples, HRM based detection aligned with disease status, accurately identifying C. ilicicola in symptomatic plants and no detection in asymptomatic tissues. Overall, this HRM assay provides a rapid, sensitive, and reliable diagnostic tool for routine molecular detection of C. ilicicola.

pathology↗

bioRxiv2026

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↗

bioRxiv2026

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↗

bioRxiv2021

Spatial transcriptomics reveals antiparasitic targets associated with essential behaviors in the human parasite Brugia malayi

Lymphatic filariasis (LF) is a chronic debilitating neglected tropical disease (NTD) caused by mosquito-transmitted nematodes that afflicts over 60 million people. Control of LF relies on routine mass drug administration with antiparasitics that clear circulating larval parasites but are ineffective against adults. The development of effective adulticides is hampered by a poor understanding of the processes and tissues driving parasite survival in the host. The adult filariae head region contains essential tissues that control parasite feeding, sensory, secretory, and reproductive behaviors, which express promising molecular substrates for the development of antifilarial drugs, vaccines, and diagnostics. We have adapted spatial transcriptomic approaches to map gene expression patterns across these prioritized but historically intractable head tissues. Spatial and tissue-resolved data reveal distinct biases in the origins of known drug targets and secreted antigens. These data were used to identify potential new drug and vaccine targets, including putative hidden antigens expressed in the alimentary canal, and to spatially associate receptor subunits belonging to druggable families. Spatial transcriptomic approaches provide a powerful resource to aid gene function inference and seed antiparasitic discovery pipelines across helminths of relevance to human and animal health.

microbiology↗

bioRxiv2019

Stress-induced dendritic branching in C. elegans requires both common arborization effectors and stress-responsive molecular pathways.

Stress influences the shape of dendritic arbors in neurons. During the stress-induced dauer stage of Caenorhabditis elegans, the IL2 neurons arborize to cover the anterior body wall. In contrast, the FLP neurons arborize to cover the anterior body wall during non-dauer development. Previous work showed that the membrane-bound receptor DMA-1 regulates FLP branching as part of a larger protein complex. Using forward genetics, we show that the IL2 neurons also use the DMA-1 complex to regulate branching. To understand the coordination of the IL2s and FLPs we conducted a time-course examination of FLPs and found previously undescribed branching patterns indicating a neighborhood effect wherein the FLPs and IL2s in the anterior have differential branching compared to the more posteriorly located PVD arborizing neurons. To determine how the IL2s and FLPs differentially regulate branching, we examined several regulators of DMA-1 localization. We show that the unfolded protein response sensor IRE-1, required for FLP branching, is only required for dauer-specific branching at elevated temperatures. Interestingly, we found that ire-1 mutants have broad, organism-wide temperature-dependent effects on dauer remodeling, suggesting a previously undescribed role for IRE-1 in phenotypic plasticity. We also found that defects in other regulators of dauer remodeling including DAF-16/FOXO, DAF-9/Cytochrome P450, and DAF-18/PTEN are required for proper IL2 arborization, but dispensable for FLP branching. Interestingly, we find that TOR adaptor protein DAF-15/RAPTOR is both required for promoting IL2 branching and inhibiting precocious development of the FLPs. Our results demonstrate specific genotypic by environmental interactions regulating dendrite arborization.\n\nSIGNIFICANCE STATEMENTNeurons have extensions called dendrites that receive information. Dendrites are often elaborately shaped with many branches. Adverse stress can reduce branching in some neurons, while increasing it in others. How stress can cause some neurons to change shape is unclear. We previously found a set of neurons in the head of the well-studied roundworm C. elegans that undergo reversible branching following exposure to specific adverse environmental conditions. Using various genetic tools, we find that branching in these neurons is controlled by a combination of branching genes common to many neuron types and others that only regulate branching in stress-responsive neurons. Our data demonstrate how experiencing stress acts through genetics pathways to cause changes to specific neurons.

neuroscience↗