Research Article

RNA interference of MRCK‐1 in Caenorhabditis elegans to explore oxidative stress responses (802.26)

Published: 2014-4

Journal: The FASEB Journal

DOI: 10.1096/fasebj.28.1_supplement.802.26

Abstract

TheCaenorhabditis elegansmyotonic dystrophy kinase‐related, Cdc42 binding kinase (MRCK‐1) is activated by the Rho GTPase CDC‐42 (cell division control protein 42), which contains a conserved redox‐sensitive sequence motif on the phosphoryl binding loop. If reactive oxygen species (ROS) can activate CDC‐42, MRCK‐1 may be required to elicit a downstream response to oxidative stress. To test this,mrck‐1expression was targeted using two RNA interference (RNAi) constructs in transgenic lines ofC. elegansthat produce green fluorescent protein (GFP) driven by redox‐sensitive promoters. After heat‐shock and chemically‐induced oxidative stress, GFP expression levels were quantified using epifluorescent microscopy. Preliminary data from heat‐shock protein reporter strain CL2070 (hsp‐16.2:GFP) indicate no significant GFP expression changes in the RNAi‐treated worms before or after heat stress, but further studies with different oxidative stressors and reporter strains are underway. If reduction ofmrck‐1is found to affect oxidative stress responses, a new mechanism for prevention of degenerative diseases and aging could be suggested. Grant Funding Source: Supported by the Henson Undergraduate Research fund.

Faculty Members

  • Patti Erickson - Biological Sciences Salisbury University Salisbury MD United States
  • Michael Robben - Biological Sciences Salisbury University Salisbury MD United States

Themes

  • Oxidative stress response
  • Transgenic model organisms in biomedical research
  • Role of kinases in cellular processes
  • Gene regulation through RNA interference
  • Mechanisms related to degenerative diseases and aging

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