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Resources » Paper

Kamat, Shaunak et al. (2011) International Worm Meeting "In vitro and in vivo investigation of modulators of hyperactivated ion channel induced necrosis in C. elegans."

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  • Comments on Kamat, Shaunak et al. (2011) International Worm Meeting "In vitro and in vivo investigation of modulators of hyperactivated ion channel induced necrosis in C. elegans." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00039501

    Kamat, Shaunak, Yeola, Shrutika, Zhang, Wenying, & Driscoll, Monica (2011). In vitro and in vivo investigation of modulators of hyperactivated ion channel induced necrosis in C. elegans presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Exposure of tissue to extreme temperature, corrosive chemicals, ischemia or other noxious stimuli can induce necrotic degeneration that is characterized by cellular swelling, loss of organellar integrity, accumulation of reactive oxygen species, activation of proteases and ultimately cell lysis. Necrosis can be genetically induced in C. elegans neurons by expression of mutant hyperactive ion channels. Mutant DEG/ENaC channels cause entry of excess calcium into the cell, triggering release of ER calcium stores and subsequent activation of calpain proteases. Due to the role of calcium in the induction and progression of this type of necrotic cell death we screened genes that encode calcium binding proteins and assayed for potential modulation of the cell death phenotype. RNAi and deletion mutant data indicate the involvement of EF hand-containing proteins localized to ER and mitochondria in the progression through necrosis. We will report on progress in deciphering details of their contributions to cell death. To extend mechanistic dissection, we have also been studying properties of hyperactivated ion channel-induced necrosis in C. elegans embryonic cell culture and find that cultured neurons behave similarly to their counterparts in vivo. We have been pioneering the use of total internal reflection fluorescence microscopy to measure the MEC-4/MEC-10 channel at the neuron surface. We find changes in the surface expression and distribution of mechanotransduction complex proteins when necrosis is induced using a temperature-sensitive mec-4(d) allele. We are also studying the effects of mutant DEG/ENaC channels on mitochondrial morphology by imaging mitochondrially localized GFP in vitro and in vivo, as data suggest a relationship between maintenance of mitochondrial integrity and susceptibility to necrotic stimuli.

    Affiliation:
    - Molecular Biol & Biochem, Rutgers Univ, Piscataway, NJ., New Jersey


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