TAF-4 is required for the life extension of isp-1, clk-1 and tpk-1 Mit mutants

Maruf H. Khan, Melissa Ligon, Lauren R. Hussey, Bryce Hufnal, Robert Farber, Erin Munkácsy, Amanda Rodriguez, Andy Dillow, Erynn Kahlig, Shane L. Rea

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


While numerous life-extending manipulations have been discovered in the nematode Caenorhabditis elegans, one that remains most enigmatic is disruption of oxidative phosphorylation. In order to unravel how such an ostensibly deleterious manipulation can extend lifespan, we sought to identify the ensemble of nuclear transcription factors that are activated in response to defective mitochondrial electron transport chain (ETC) function. Using a feeding RNAi approach, we targeted over 400 transcription factors and identified 15 that, when reduced in function, reproducibly and differentially altered the development, stress response, and/or fecundity of isp-1(qm150) Mit mutants relative to wild-type animals. Seven of these transcription factors - AHA-1, CEH-18, HIF-1, JUN-1, NHR-27, NHR-49 and the CREB homolog-1 (CRH-1)- interacting protein TAF-4 - were also essential for isp-1 life extension. When we tested the involvement of these seven transcription factors in the life extension of two other Mit mutants, namely clk-1(qm30) and tpk-1(qm162), TAF-4 and HIF- 1 were consistently required. Our findings suggest that the Mit phenotype is under the control of multiple transcriptional responses, and that TAF-4 and HIF-1 may be part of a general signaling axis that specifies Mit mutant life extension.

Original languageEnglish (US)
Pages (from-to)741-758
Number of pages18
Issue number10
StatePublished - Oct 2013


  • Aha-1
  • C.elegans
  • Ceh-18
  • Clk-1
  • Hif-1
  • Isp-1
  • Jun-1
  • Lifespan
  • Mit mutants
  • Mitochondria
  • Nhr-27
  • Nhr-49
  • Taf-4

ASJC Scopus subject areas

  • Aging
  • Cell Biology


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