C. elegans SISS-1 is an Epidermal Growth Factor (EGF) family ligand that signals from damaged cells to sleep-promoting neurons during s tress- i nduced s leep (SIS). Damage to a range of tissues can trigger SIS, and we reasoned that siss-1 should be widely expressed. Here we investigate siss-1 expression using both endogenous and transgenic fluorescent reporters. Our endogenous reporter reveals siss-1 expression in the pharynx, gut, rectal gland, vulval muscles, and a subset of neurons. Our transgenic reporters reveal expression in additional cell types including the distal tip cell of the migrating gonad and vulF cells of the developing vulva. This expression is specific relative to our expectation and suggests that not all tissues are capable of signaling to sleep neurons.

Post-translational modifications (PTMs) of tubulin regulate microtubule properties and functions. The Verhey lab created recombinant monoclonal antibodies (rMAbs) against tubulin acetylation (rMAb-6-11B-1), tyrosinated α-tubulin (rMAb-YL1/2), and glutamylation (rMAb-GT335) (Blasius et al., 2025; Hotta et al., 2026). Here, we validate these rMAbs in C. elegans hermaphrodites and males. These rMAbs faithfully reproduce the reported cell-type-specific staining patterns of commercial antibodies, providing high-quality, cost-effective resources for studying the tubulin code.

Transcription factor nucleocytoplasmic dynamics play a key role in developmental gene regulation. In Dictyostelium , the transcription factor GtaC exhibits nucleocytoplasmic shuttling, but its shuttling trajectory across multicellular aggregation has not been systematically quantified. Using a knock-in strain, we tracked GtaC dynamics from starvation through aggregation and quantified developmental changes in shuttling period, amplitude, and synchrony. Notably, brief-pulse optogenetic activation of cAMP at higher input frequencies reproduced the reported attenuation of GtaC shuttling amplitude with high temporal precision and minimal phototoxicity. Together, long-term quantification and brief-pulse optogenetic cAMP perturbation show that GtaC nucleocytoplasmic shuttling is developmentally tuned in a frequency-dependent manner.

Bacteriophages RazzB and SwissCheezer were isolated from soil in southwestern Pennsylvania. RazzB is a cluster AP siphovirus infecting  Arthrobacter globiformis B-2979 and contains a 69,522 bp genome with 65.8% GC content, 127 predicted protein-coding genes and no tRNAs. SwissCheezer is a cluster EK phage with a podovirus morphology infecting Microbacterium foliorum NRRL B-24224 and contains a 53,956 bp genome with 60.0% GC content and 54 predicted protein-coding genes.

The Caenorhabditis Intervention Testing Program aims to identify lifespan-extending interventions that are effective across diverse genetic backgrounds. Previous studies identified a role for anticonvulsants in lifespan extension in the nematode Caenorhabditis elegans . The FDA-approved anticonvulsant levetiracetam acts in C. elegans and modulates neurotransmission. However, levetiracetam effects on nematode lifespan are unknown. Here, we examine the effect of levetiracetam on the lifespan of strain representatives from three species of the Caenorhabditis genus. Our results do not reveal an effect of levetiracetam on nematode lifespan, indicating that anticonvulsants can differ in their ability to extend lifespan.

We previously reported that triazine thiols reduce apolipoprotein B (ApoB) secretion from human iPSC-derived hepatocytes (HLCs) and from humanized mice. To determine whether these compounds affected hepatocyte mRNA levels, we performed bulk RNA sequencing of HLCs treated with the triazine thiol DL-1 or with vehicle (DMSO) for 24 hours. Analyses revealed that in triazine thiol-treated cells, 145 mRNAs were reduced and 37 increased by ≥ 2-fold.  Several mRNAs encoding cysteine-rich metallothionines were upregulated, implying that HLCs respond to treatment by mounting a protective response through metal buffering.

Antibiotic resistance is a severe problem stemming from the overuse of antibiotics. Manuka honey, a unique honey from New Zealand, may serve as an alternative to traditional antibiotics for treating bacterial infections. A transgenic line of Caenorhabditis elegans , hlh-30 ::3xFLAG::eGFP, was utilized as a stress reporter strain to quantify changes in GFP expression associated with host response to S. aureus infection and honey treatment. Imaging, longevity, and developmental assays all demonstrated that manuka honey reduced the host stress response to S. aureus infection in C. elegans . These findings suggest that manuka honey may be effective against S. aureus infections.

Protein quality control (QC) safeguards cellular proteostasis by directing misfolded proteins for degradation via the ubiquitin-proteasome system. QC is compartmentalized within cells, and the key proteins involved in the turnover of cytosolic proteins with mutations in mammalian cells are not well defined. Using a fluorescent reporter assay that provides a readout for protein stability, we examined the contributions of known QC E3 ligases (STUB1, UBE2O, UBR4, UBR5, and HUWE1) on the turnover of disease-associated missense variants. Loss of individual ligases did not consistently stabilize substrates, indicating that none of these E3s appear to broadly recognize missense mutant proteins.

The complete genome of LordLeafolot, a subcluster C1 virus displaying the myovirus morphology and infecting Mycobacterium smegmatis mc²155, is 155,266 bp and encodes 235 predicted proteins, 32 tRNAs, and one tmRNA. The lack of identifiable integrase and repressor genes, along with failed attempts to establish lysogeny, indicates that LordLeafolot has a strictly lytic life cycle.

Microtubule dynamics influence neuron morphogenesis. We investigated the role of the conserved microtubule-associated protein Mini Spindles (Msps) in the morphogenesis of branched dendrite arbors using Drosophila melanogaster larval class III and class IV dendritic arborization neurons as two models of branch organization. In both classes, knocking down msps expression reduced dendrite branching but increased terminal dendrite length. In msps RNAi class IV da neurons, dendrite growth failed to scale in proportion to increasing larval size between the second and third instar. These results suggest that Msps is required for the dynamic expansion of dendrite arbors during periods of rapid organismal growth.