Transgenerational Inheritance of Pathogen Avoidance or: How Getting Food Poisoning Might Save Your Species

  • Speaker
  • Coleen MurphyColeen T. Murphy, Ph.D.James A. Elkins, Jr. Professor in the Life Sciences, Princeton University
Date & Time

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Our experiences influence our decisions, but can they influence our descendants’ decisions? Animals must distinguish pathogens from nutritious food sources; this is particularly challenging for C. elegans, which must distinguish bacterial food from pathogens among the many bacteria in its environment.

In this lecture, Coleen Murphy will present how she and her colleagues found that a single exposure to purified small RNAs isolated from pathogenic Pseudomonas aeruginosa (PA14) is sufficient to induce pathogen avoidance in the treated worms and four subsequent generations of progeny. The RNA interference (RNAi) and PIWI-interacting RNA (piRNA) pathways, the germline and the ASI neuron are all required for avoidance behavior induced by bacterial small RNAs and for the transgenerational inheritance of this behavior. A single P. aeruginosa non-coding RNA, P11, is necessary and sufficient to convey learned avoidance of PA14, and its C. elegans target, maco-1, is required for avoidance. Their results suggest that this non-coding-RNA-dependent mechanism evolved to survey the microbial environment of the worm, use this information to make appropriate behavioral decisions and pass this information on to its progeny.

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About the Speaker

Coleen Murphy

Murphy graduated from the University of Houston with a B.S. in biochemistry and biophysics and earned her doctorate in biochemistry at Stanford University. She then did her postdoctoral work at the University of California, San Francisco, where she identified the set of genes downstream of the insulin signaling/FOXO longevity pathway. She is the James A. Elkins, Jr. professor in the life sciences at Princeton University and director of the Simons Collaboration on Plasticity and the Aging Brain.

Murphy’s team has developed C. elegans models of human “quality of life” aging phenotypes, including cognitive aging and reproductive aging. She and her colleagues have also identified remarkably well-conserved genetic pathways that can extend these processes with age.

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