6533b872fe1ef96bd12d385f

RESEARCH PRODUCT

Plasma membrane Ca2+ ATPase 4 is required for sperm motility and male fertility.

Angel L. ArmesillaDelvac OceandyKlaus-peter KnobelochKai SchuhJudith C. WilliamsMichael EmersonLudwig NeysesJürgen LiebermannEriks JankevicsKarin BundschuElizabeth J. Cartwright

subject

MaleTime FactorsBiochemistryMiceTestisProtein IsoformsCloning MolecularCation Transport Proteinsreproductive and urinary physiologySperm motilityMice KnockoutRecombination GeneticReverse Transcriptase Polymerase Chain ReactionPlasma Membrane Calcium-Transporting ATPasesFluoresceinsTransport proteinCell biologyBlotting SouthernBiochemistrySperm Motilityendocrine systemDNA ComplementaryGenotypeBlotting WesternMolecular Sequence Datachemistry.chemical_elementSuccinimidesCalcium-Transporting ATPasesFertilization in VitroCalciumBiologyPlasma Membrane Calcium-Transporting ATPasesAnimalsHumansMolecular BiologyFluorescent DyesCalcium metabolismModels Geneticurogenital systemCell BiologyBlotting NorthernSpermProtein Structure TertiaryRatsCalcium ATPaseAlternative SplicingFertilitychemistryMicroscopy FluorescencePlasma membrane Ca2+ ATPaseCalcium

description

Calcium and Ca(2+)-dependent signals play a crucial role in sperm motility and mammalian fertilization, but the molecules and mechanisms underlying these Ca(2+)-dependent pathways are incompletely understood. Here we show that homozygous male mice with a targeted gene deletion of isoform 4 of the plasma membrane calcium/calmodulin-dependent calcium ATPase (PMCA), which is highly enriched in the sperm tail, are infertile due to severely impaired sperm motility. Furthermore, the PMCA inhibitor 5-(and-6)-carboxyeosin diacetate succinimidyl ester reduced sperm motility in wild-type animals, thus mimicking the effects of PMCA4 deficiency on sperm motility and supporting the hypothesis of a pivotal role of the PMCA4 on the regulation of sperm function and intracellular Ca(2+) levels.

10.1074/jbc.m312599200https://pubmed.ncbi.nlm.nih.gov/15078889