Publications by authors named "E R Troemel"

Microsporidia are common natural pathogens of the nematode . Infection of by the microsporidian species leads to induction of the Intracellular Pathogen Response (IPR), including transcriptional upregulation of 26 genes. The divergent ' ' sequence signature is conserved with humans, but PALS proteins have unknown biochemical functions.

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Upon sensing viral RNA, mammalian RIG-I-like receptors (RLRs) activate downstream signals using caspase activation and recruitment domains (CARDs), which ultimately promote transcriptional immune responses that have been well studied. In contrast, the downstream signaling mechanisms for invertebrate RLRs are much less clear. For example, the RLR DRH-1 lacks annotated CARDs and up-regulates the distinct output of RNA interference.

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Orsay virus infection in the nematode Caenorhabditis elegans presents an opportunity to study host-virus interactions in an easily culturable, whole-animal host. Previously, a major limitation of C. elegans as a model for studying antiviral immunity was the lack of viruses known to naturally infect the worm.

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Article Synopsis
  • Heat shock is a serious stressor, and researchers studied how a specific ubiquitin ligase complex, CUL-6, helps the nematode C. elegans survive this stress.
  • The study found that CUL-6 enhances thermotolerance by promoting the degradation of the heat shock protein HSP-90 specifically in the intestine.
  • The effectiveness of CUL-6 in improving survival during heat shock relies on proper lysosomal function, as it directs HSP-90 to lysosome-related organelles for degradation.
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Protein quality control pathways play important roles in resistance against pathogen infection. For example, the conserved transcription factor SKN-1/NRF up-regulates proteostasis capacity after blockade of the proteasome and also promotes resistance against bacterial infection in the nematode Caenorhabditis elegans. SKN-1/NRF has 3 isoforms, and the SKN-1A/NRF1 isoform, in particular, regulates proteasomal gene expression upon proteasome dysfunction as part of a conserved bounce-back response.

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