A Calcineurin Homologous Protein Is Required For Sodium-proton Exchange Events In The C. Elegans Intestine

Title:
A Calcineurin Homologous Protein Is Required For Sodium-proton Exchange Events In The C. Elegans Intestine
Authors:
Wagner, Jamie; Allman, Erik; Taylor, Ashley; Ulmschneider, Kiri; Kovanda, Timothy; Ulmschneider, Bryne; Nehrke, Keith; Peters, Maureen A.
Abstract:
Caenorhabditis elegans defecation is a rhythmic behavior, composed of three sequential muscle contractions, with a 50-s periodicity. The motor program is driven by oscillatory calcium signaling in the intestine. Proton fluxes, which require sodium-proton exchangers at the apical and basolateral intestinal membranes, parallel the intestinal calcium flux. These proton shifts are critical for defecation-associated muscle contraction, nutrient uptake, and longevity. How sodium-proton exchangers are activated in time with intestinal calcium oscillation is not known. The posterior body defecation contraction mutant (pbo-1) encodes a calcium-binding protein with homology to calcineurin homologous proteins, which are putative cofactors for mammalian sodium-proton exchangers. Loss of pbo-1 function results in a weakened defecation muscle contraction and a caloric restriction phenotype. Both of these phenotypes also arise from dysfunctions in pH regulation due to mutations in intestinal sodium-proton exchangers. Dynamic, in vivo imaging of intestinal proton flux in pbo-1 mutants using genetically encoded pH biosensors demonstrates that proton movements associated with these sodium-proton exchangers are significantly reduced. The basolateral acidification that signals the first defecation motor contraction is scant in the mutant compared with a normal animal. Luminal and cytoplasmic pH shifts are much reduced in the absence of PBO-1 compared with control animals. We conclude that pbo-1 is required for normal sodium-proton exchanger activity and may couple calcium and proton signaling events.
Citation:
Wagner, Jamie, Erik Allman, Ashley Taylor, Kiri Ulmschneider, et al. 2011. "A Calcineurin Homologous Protein Is Required For Sodium-proton Exchange Events In The C. Elegans Intestine." American Journal Of Physiology.cell Physiology 301(6): 1389-403.
Publisher:
American Physiological Society
DATE ISSUED:
2011-12
Department:
Biology
Type:
article
PUBLISHED VERSION:
10.1152/ajpcell.00139.2011
PERMANENT LINK:
http://hdl.handle.net/11282/310111

Full metadata record

DC FieldValue Language
dc.contributor.authorWagner, Jamieen_US
dc.contributor.authorAllman, Eriken_US
dc.contributor.authorTaylor, Ashleyen_US
dc.contributor.authorUlmschneider, Kirien_US
dc.contributor.authorKovanda, Timothyen_US
dc.contributor.authorUlmschneider, Bryneen_US
dc.contributor.authorNehrke, Keithen_US
dc.contributor.authorPeters, Maureen A.en_US
dc.date.accessioned2013-12-23T16:25:37Z-
dc.date.available2013-12-23T16:25:37Z-
dc.date.issued2011-12en
dc.identifier.citationWagner, Jamie, Erik Allman, Ashley Taylor, Kiri Ulmschneider, et al. 2011. "A Calcineurin Homologous Protein Is Required For Sodium-proton Exchange Events In The C. Elegans Intestine." American Journal Of Physiology.cell Physiology 301(6): 1389-403.en_US
dc.identifier.issn1522-1563en_US
dc.identifier.urihttp://hdl.handle.net/11282/310111-
dc.description.abstractCaenorhabditis elegans defecation is a rhythmic behavior, composed of three sequential muscle contractions, with a 50-s periodicity. The motor program is driven by oscillatory calcium signaling in the intestine. Proton fluxes, which require sodium-proton exchangers at the apical and basolateral intestinal membranes, parallel the intestinal calcium flux. These proton shifts are critical for defecation-associated muscle contraction, nutrient uptake, and longevity. How sodium-proton exchangers are activated in time with intestinal calcium oscillation is not known. The posterior body defecation contraction mutant (pbo-1) encodes a calcium-binding protein with homology to calcineurin homologous proteins, which are putative cofactors for mammalian sodium-proton exchangers. Loss of pbo-1 function results in a weakened defecation muscle contraction and a caloric restriction phenotype. Both of these phenotypes also arise from dysfunctions in pH regulation due to mutations in intestinal sodium-proton exchangers. Dynamic, in vivo imaging of intestinal proton flux in pbo-1 mutants using genetically encoded pH biosensors demonstrates that proton movements associated with these sodium-proton exchangers are significantly reduced. The basolateral acidification that signals the first defecation motor contraction is scant in the mutant compared with a normal animal. Luminal and cytoplasmic pH shifts are much reduced in the absence of PBO-1 compared with control animals. We conclude that pbo-1 is required for normal sodium-proton exchanger activity and may couple calcium and proton signaling events.en_US
dc.publisherAmerican Physiological Societyen_US
dc.identifier.doi10.1152/ajpcell.00139.2011-
dc.subject.departmentBiologyen_US
dc.titleA Calcineurin Homologous Protein Is Required For Sodium-proton Exchange Events In The C. Elegans Intestineen_US
dc.typearticleen_US
dc.identifier.journalAmerican Journal Of Physiology - Cell Physiologyen_US
dc.subject.keywordCaloric restrictionen_US
dc.subject.keywordCaenorhabditis elegansen_US
dc.subject.keywordMotor programen_US
dc.subject.keywordRhythmic behavioren_US
dc.subject.keywordDefecationen_US
dc.identifier.volume301en_US
dc.identifier.issue6en_US
dc.identifier.startpage1389en_US
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