What governs how fast we age? Why do some biological processes stop working earlier than others? And what is happening at the molecular and cellular level as some organisms age while others continue to thrive?

Although seemingly philosophical in nature, these questions address one of the major mysteries of biology, the process of aging. With recent developments in genetics, molecular biology, and genomics, we now have the possibility of addressing these questions at the molecular level. Because our ultimate goal is not simply to extend lifespan, but to improve overall health, we must identify the genes associated with biological functions that we typically associate with quality of life. The goal of our laboratory's work is to understand the molecular mechanisms governing longevity and maintenance of the biological processes that exhibit age-related decline.

Recent Publications

  • Cross-kingdom recognition of bacterial small RNAs induces transgenerational pathogenic avoidance

    Rachel Kaletsky; Rebecca S. Moore; Lance L. Parsons; Coleen T. Murphy
    Journal Article
  • Gut feelings: microRNAs tune protein quality control and ageing to odours

    Rachel Kaletsky; Coleen T. Murphy
    Journal Article

    A new study in C. elegans identifies a microRNA-dependent mechanism that enables olfactory neurons to rapidly regulate protein degradation in the intestine and therefore organismal ageing.

  • Insulin-like peptides and the mTOR-TFEB pathway protect \textitCaenorhabditis elegans hermaphrodites from mating-induced death

    Cheng Shi; Lauren N. Booth; Coleen T. Murphy
    Journal Article

    Lifespan is shortened by mating, but these deleterious effects must be delayed long enough for successful reproduction. Susceptibility to brief mating-induced death is caused by the loss of protection upon self-sperm depletion. Self-sperm maintains the expression of a DAF-2 insulin-like antagonist, INS-37, which promotes the nuclear...

    insulin signaling; lifespan; mating; mTOR; TFEB
  • Investigating Mechanisms that Control Ubiquitin-Mediated DAF-16/FOXO Protein Turnover.

    Thomas Heimbucher; Coleen T. Murphy
    Journal Article

    Protein turnover of FOXO family transcription factors is regulated by the ubiquitin-proteasome system. A complex interplay of factors that covalently attach certain types of ubiquitin chains (E3-ubiquitin ligases), and enzymes that are able to remove ubiquitin conjugates (deubiquitylases), regulate the degradation of FOXO proteins by the...

  • The nematode Caenorhabditis elegans as a model for aging research

    HID Mack; T Heimbucher; C.T. Murphy
    Journal Article
  • A PBX/MEIS Complex Balances Reproduction and Somatic Resilience

    T Heimbucher; CT Murphy
    Journal Article
  • Piwi/PRG-1 Argonaute and TGF-β Mediate Transgenerational Learned Pathogenic Avoidance

    Rebecca S. Moore; Rachel Kaletsky; Coleen T. Murphy
    Journal Article

    The ability to inherit learned information from parents could be evolutionarily beneficial, enabling progeny to better survive dangerous conditions. We discovered that, after C. elegans have learned to avoid the pathogenic bacteria Pseudomonas aeruginosa (PA14), they pass this learned behavior on to their progeny, through either the male or...

  • Profiling of presynaptic mRNAs reveals a role for axonal PUMILIOs in associative memory formation

    Rachel Arey; Rachel Kaletsky; Coleen T. Murphy
    Journal Article

    Presynaptic protein synthesis is important in the adult central nervous system; however, the set of mRNAs localized to presynaptic areas has yet to be identified in any organism. We differentially labeled somatic and synaptic compartments nervous system-wide in adult C. elegans and isolated synaptic regions for deep sequencing. Analysis of the...

  • ZIP-5/bZIP transcription factor regulation of folate metabolism is critical for aging axon regeneration

    Vanisha Lakhina; Melanie McReynolds; Daniel T. Grimes; Joshua D. Rabinowitz; Rebecca D. Burdine; Coleen T. Murphy
    Journal Article

    Aging is associated with reduced capacity for tissue repair, perhaps the most critical of which is a decline in the ability of aged neurons to recover after injury. Identifying factors that improve the regenerative ability of aging neurons is a prerequisite for therapy design and remains an enormous challenge, yet many of the genes that play a...

  • Activation of G Signaling Enhances Memory Consolidation and Slows Cognitive Decline.

    Rachel N. Arey; Geneva M. Stein; Rachel Kaletsky; Amanda Kauffman; Coleen T. Murphy
    Journal Article

    Perhaps the most devastating decline with age is the loss of memory. Therefore, identifying mechanisms to restore memory function with age is critical. Using C. elegans associative learning and memory assays, we identified a gain-of-function G signaling pathway mutant that forms a long-term (cAMP response element binding protein [CREB]-...

Contact information

Carl Icahn Lab 148
Princeton University
Princeton NJ, 08540

Lab phone: 609-258–9505

Coleen Murphy

  • Professor of Molecular Biology and the Lewis-Sigler Institute for Integrative Genomics
  • Director of the Paul F. Glenn Laboratories for Aging Research at Princeton University
Phone: 609-258–9396

Dawn Capizzi

  • Faculty Assistant
Phone: 609-258–1617