Emily R. Troemel

This study shows that C. elegans STA-1, a STAT-like protein, relocalizes from nuclei to cytoplasm during viral infection, acting cell-intrinsically to repress anti-viral defense.

This study identifies LET-418 as a regulator of intracellular pathogen response in C. elegans intestine by analyzing its target genes and functional effects on immune response genes.

This study identifies PALS-22 and PALS-25 as mitochondrial proteins in C. elegans that regulate mitochondrial fragmentation to enhance immunity against intracellular pathogens.

The paper maps the functional importance of site-specific ubiquitination across the human proteome by analyzing conservation, perturbation, and machine learning scores.

The paper identifies PALS-22 as a regulator of AGO expression in C. elegans, showing its role in balancing immunity and germline health through modulation of RNAi and epigenetic inheritance.

The paper identifies chromatin regulators in C. elegans that repress immune responses to intracellular pathogens, linking developmental regulation to immune control.

This study identifies DRH-1 as a C. elegans RIG-I-like receptor that uses 2CARD domains to activate anti-viral immunity in intestinal cells, showing parallels with mammalian RIG-I signaling.

This study shows that CUL-6 ubiquitin ligase promotes thermotolerance by degrading HSP-90 in intestinal lysosomes, independent of HSF-1.

The paper investigates gene expression of Nematocida microsporidia and host responses in Caenorhabditis nematodes, finding conserved transcriptional patterns across hosts and microsporidia species.

This paper introduces a NanoLuc-based method for highly sensitive gene expression detection in C. elegans, showing it can detect signals at 400,000-fold over background in populations and from single worms.

This study identifies two C. elegans-specific genes, pals-22 and pals-25, which function as antagonistic regulators controlling the switch between growth and pathogen resistance.

This study identifies a novel pathway, the Intracellular Pathogen Response (IPR), that promotes proteostasis in C. elegans by upregulating ubiquitin ligase components like cul-6, with pals-22 acting as a repressor.