ArticlePLoS pathogens2026
RNA methyltransferase CMTR-1 inhibition activates a GATA transcription factor-mediated protective immune response.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Organisms can activate innate immunity not only by detecting pathogens but also by sensing disturbances to essential cellular processes. Such damage-based surveillance provides a means to identify cellular disruptions that prime host immunity even in the absence of infection. To uncover pathways that enhance immunity, we perform a forward genetic screen in Caenorhabditis elegans for mutants with elevated intestinal immune activation. This screen identifies a hypomorphic allele of the conserved mRNA cap 2'-O-methyltransferase cmtr-1, which strongly induces immune effector expression. Transcriptomic profiling reveals the broad activation of innate immune responses, and functional analyses demonstrate that this response requires the GATA transcription factor ELT-2. Notably, loss of cmtr-1 increases resistance to Pseudomonas aeruginosa, indicating that reduced RNA cap methylation can elicit protective immunity. Together, these findings reveal a previously unrecognized mechanism of immune surveillance and demonstrate that perturbation of CMTR-1 serves as a danger signal, triggering an ELT-2-dependent protective immune response.
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