Biology subjects

Schwartz, H. T.

Publications and source records attributed to Schwartz, H. T..

6 recordsLinked to original sources

bioRxiv2026

A nematode-trapping fungus orchestrates polarity cues, septins, and NOX signaling for trap formation

The ability to reprogram cell morphogenesis in response to environmental cues is fundamental to microbial adaptation and survival. The nematode-trapping fungus Arthrobotrys oligospora exemplifies this plasticity by developing adhesive traps to capture nematodes. This morphological transition involves spatial reorientation of cell polarity, cytoskeletal remodeling, and cell fusion. However, the molecular mechanisms that coordinate these processes remain unclear. Using live-cell imaging, genetics, and functional assays, we demonstrated that cell polarity proteins localize to hyphal tips to direct growth, while actin and septins assemble at the curving inner rim to shape trap architecture. Conserved NADPH oxidases are induced by the presence of nematodes and are required for the recruitment of cell polarity proteins and cytoskeletal factors to promote trap cell fusion. Together, these findings reveal that polarity cues, cytoskeletal organization, and reactive oxygen species signaling are integrated to orchestrate nematode-induced trap development, establishing nematode-trapping fungi as a versatile model to study fungal cell biology.

cell biology↗

bioRxiv2026

Ammonium Transporters Govern Nutrient Sensing and Trap Induction in the Nematode-Trapping Fungi Arthrobotrys oligospora

To survive nutrient scarcity, organisms must detect environmental cues and acquire essential resources efficiently. Under nutrient-limiting conditions, nematode-trapping fungi (NTF) such as Arthrobotrys oligospora form specialized traps to capture nematodes; this transition can be suppressed by the ready availability of carbon and nitrogen. Ammonium transporters of the MEP family are key regulators of nitrogen sensing and uptake across all forms of life. We identified three MEP genes in A. oligospora based on protein sequence homology. Functional assays revealed that loss of the MEP genes alters the funguss ability to produce traps, without affecting the morphology of the traps or their ability to function in catching nematodes. Heterologous expression in Saccharomyces cerevisiae revealed functional conservation of Mep transporter subclasses. Together, the Mep transporters of A. oligospora contribute to ammonium-regulated trap induction.

genetics↗

bioRxiv2025

Evolution of parasitism-related traits in nematodes

The abundant resources provided by the host provide an evolutionary rationale for parasitism and drive the metabolic and developmental divergence of parasitic and free-living animals. Two evolutionarily distant nematode genera, Steinernema and Heterorhabditis, independently evolved an entomopathogenic lifestyle, in which they invade insects and kill them with the assistance of specifically associated symbiotic pathogenic bacteria. It had been generally assumed that the worms, being bacterivores, feed on their symbiotic bacteria, which rapidly reproduce as they consume the insect host. The evolutionary adaptations of entomopathogenic nematodes to a parasitic lifestyle developmentally, and the symbiotic relationships of entomopathogenicity, remain largely unknown. We developed an axenic culture medium that supports robust and sustained growth of Steinernema hermaphroditum, with finite control of nutrients available to the nematodes. We found that, uniquely among the nematodes tested, S. hermaphroditum hatchlings cannot endure in a nutrient-poor environment; this ability is impaired but still present in Heterorhabditis bacteriophora. Similarly, the ability to forage for food is completely lost in H. bacteriophora hatchlings and severely compromised in S. hermaphroditum. We reasoned that these traits were lost because they are unnecessary to obligate parasites that always hatch in a resource-rich host. We further found that Steinernema and, to a limited extent, Heterorhabditis nematodes can successfully invade, develop, and reproduce inside a living insect host independent of their symbiotic bacteria, apparently feeding on the hemolymph, and emerge carrying bacteria found within, explaining the evolutionary origins of entomopathogenic nematodes. HighlightsO_LIA simple but robust axenic culturing method for the emerging model nematode Steinernema hermaphroditum and other nematode parasites of invertebrates. C_LIO_LINematode adaptation to parasitism is associated with changes in modes of feeding. C_LIO_LIConvergent evolution led to the loss of hatchling survival traits in entomopathogenic nematodes. C_LIO_LIEntomopathogenic nematodes evolved from parasitoid ancestors and likely acquired their bacterial symbionts from their hosts. C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=146 HEIGHT=200 SRC="FIGDIR/small/678730v2_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@880785org.highwire.dtl.DTLVardef@a5cbcforg.highwire.dtl.DTLVardef@e78671org.highwire.dtl.DTLVardef@2b9d99_HPS_FORMAT_FIGEXP M_FIG C_FIG

evolutionary biology↗

bioRxiv2025

Genomes of the entomopathogenic nematode Steinernema hermaphroditum and its associated bacteria

As an entomopathogenic nematode (EPN), Steinernema hermaphroditum parasitizes insect hosts and harbors symbiotic Xenorhabdus griffinae bacteria. In contrast to other Steinernematids, S. hermaphroditum has hermaphroditic genetics, offering the experimental scope found in Caenorhabditis elegans. To enable biological analysis of S. hermaphroditum, we have assembled and analyzed its reference genome. This genome assembly has five chromosomal scaffolds and 83 unassigned scaffolds totaling 90.7 Mb, with 19,426 protein-coding genes having a BUSCO completeness of 88.0%. Its autosomes show higher densities of strongly conserved genes in their centers, as in C. elegans, but repetitive elements are evenly distributed along all chromosomes, rather than with higher arm densities as in C. elegans. Either when comparing protein motif frequencies between nematode species or when analyzing gene family expansions during nematode evolution, we observed two categories of genes preferentially associated with the origin of Steinernema or S. hermaphroditum: orthologs of venom genes in S. carpocapsae or S. feltiae; and some types of chemosensory G protein-coupled receptors, despite the tendency of parasitic nematodes to have reduced numbers of chemosensory genes. Three-quarters of venom orthologs occurred in gene clusters, with the larger clusters comprising functionally diverse pathogenicity islands rather than paralogous repeats of a single venom gene. While assembling the genome of S. hermaphroditum, we coassembled bacterial genomes, finding sequence data for not only the known symbiont, X. griffinae, but also for eight other bacterial genera. All eight genera have previously been observed to be associated with Steinernema species or the EPN Heterorhabditis, and may constitute a "second bacterial circle" of EPNs. The genome assemblies of S. hermaphroditum and its associated bacteria will enable use of these organisms as a model system for both entomopathogenicity and symbiosis.

genomics↗

bioRxiv2021

The entomopathogenic nematode Steinernema hermaphroditum is a self-fertilizing hermaphrodite and a genetically tractable system for the study of parasitic and mutualistic symbiosis

Entomopathogenic nematodes, including Heterorhabditis and Steinernema, are parasitic to insects and contain mutualistically symbiotic bacteria in their intestines (Photorhabdus and Xenorhabdus, respectively) and therefore offer opportunities to study both mutualistic and parasitic symbiosis. The establishment of genetic tools in entomopathogenic nematodes has been impeded by limited genetic tractability, inconsistent growth in vitro, variable cryopreservation, and low mating efficiency. We obtained the recently described Steinernema hermaphroditum strain CS34 and optimized its in vitro growth, with a rapid generation time on a lawn of its native symbiotic bacteria Xenorhabdus griffiniae. We developed a simple and efficient cryopreservation method. Previously, S. hermaphroditum isolated from insect hosts was described as first-generation hermaphroditic and second-generation gonochoristic. We discovered that CS34, when grown in vitro, produced consecutive generations of autonomously reproducing hermaphrodites accompanied by rare males. We performed mutagenesis screens in S. hermaphroditum that produced mutant lines with visible and heritable phenotypes. Genetic analysis of the mutants demonstrated that this species reproduces by self-fertilization rather than parthenogenesis and that its sex is determined chromosomally. Genetic mapping has thus far identified markers on the X chromosome and three of four autosomes. We report that S. hermaphroditum CS34 is the first consistently hermaphroditic entomopathogenic nematode and is suitable for genetic model development to study naturally occurring mutualistic symbiosis and insect parasitism.

genetics↗

bioRxiv2018

Evolutionary analysis implicates RNA polymerase II pausing and chromatin structure in nematode piRNA biogenesis

Piwi-interacting RNAs (piRNAs) control transposable elements widely across metazoans but have rapidly evolving biogenesis pathways. In Caenorhabditis elegans, almost all piRNA loci are found within two 3Mb clusters on Chromosome IV. Each piRNA locus possesses an upstream motif that recruits RNA polymerase II to produce a [~]28 nt precursor transcript. Here, we use comparative epigenomics across nematodes to gain insight into piRNA biogenesis. We show that the piRNA upstream motif is derived from core promoter elements controlling snRNA biogenesis. We describe two alternative modes of piRNA organisation in nematodes: in C. elegans and closely related nematodes, piRNAs are clustered within repressive H3K27me3 chromatin, whilst in other species, typified by Pristionchus pacificus, piRNAs are distributed genome-wide within introns of actively transcribed genes. In both groups, piRNA production depends on downstream sequence signals associated with RNA polymerase II pausing, which synergise with the chromatin environment to control piRNA precursor transcription.

genomics↗