Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alternative Splicing
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Animals
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Blotting, Northern
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Blotting, Southern
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Blotting, Western
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Calcium / metabolism
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Calcium-Transporting ATPases / biosynthesis*
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Cation Transport Proteins
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Cloning, Molecular
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DNA, Complementary / metabolism
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Fertility*
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Fertilization in Vitro
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Fluoresceins / pharmacology
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Fluorescent Dyes / pharmacology
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Genotype
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Humans
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Male
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Mice
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Mice, Knockout
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Microscopy, Fluorescence
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Models, Genetic
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Molecular Sequence Data
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Plasma Membrane Calcium-Transporting ATPases
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Protein Isoforms
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Protein Structure, Tertiary
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Rats
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Recombination, Genetic
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Reverse Transcriptase Polymerase Chain Reaction
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Sperm Motility*
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Succinimides / pharmacology
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Testis / metabolism
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Time Factors
Substances
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5-(6)-carboxyfluorescein diacetate succinimidyl ester
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Cation Transport Proteins
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DNA, Complementary
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Fluoresceins
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Fluorescent Dyes
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Protein Isoforms
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Succinimides
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Plasma Membrane Calcium-Transporting ATPases
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Calcium-Transporting ATPases
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Calcium
Associated data
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GENBANK/AY560895
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GENBANK/AY569896