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Calcineurin homologous protein is required for a proton‐activated muscle contraction in Caenorhabditis elegans
Author(s) -
Wagner Jamie,
Taylor Ashley,
Ulmschneider Kiri,
Ulmschneider Bryne,
Nehrke Keith,
Peters Maureen A.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.815.15
Subject(s) - caenorhabditis elegans , microbiology and biotechnology , calcium , mutant , chemistry , biophysics , contraction (grammar) , biochemistry , biology , endocrinology , gene , organic chemistry
The Caenorhabditis elegans defecation cycle is a 3‐step motor program. Cycle timing is controlled by intestinal calcium flux. The first step, posterior body wall muscle contraction (pBoc), is elicited by protons 1 , 2 . Protons are transported from the intestine into the pseudocoelomic space via the sodium‐proton exchanger 7 (NHX‐7) and activate ion channels in body wall muscles, resulting in contraction 1 . A second exchanger, NHX‐2, allows proton movements between the lumen and intestinal cells 2 . We hypothesize calcineurin homologous protein (CHP), a calcium responsive co‐factor for sodium‐proton exchangers, activates these NHXs in response to calcium flux. Two CHP mutants that alter calcium binding motifs exhibit pBoc defects. Genetically encoded pH indicator proteins were used to monitor pH levels in vivo . CHP mutants display altered pseudocoelomic, cytoplasmic, and lumenal proton fluxes. Cumulatively, chp mutants' pH phenotypes encompass both nhx‐2 's and nhx‐7 's mutant traits, suggesting CHP activates these exchangers to coordinate the calcium wave and pBoc initiation. Support is from the NSF.