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#sperm motility

5 public questions tagged with this topic.

Regeneration -ll

Sperm motility in sea urchins is initiated by:

Sea urchin sperm are kept quiescent in gonads where pH is acidic and carbon dioxide high, maintaining intracellular pH around 7.2. Upon spawning into seawater pH 8.0, sodium-hydrogen exchangers extrude protons driven by sodium gradient, raising internal pH to 7.6. Alkalization activates dynein ATPase, increases mitochondrial oxygen consumption, enhances flagellar beat frequency, and sensitizes guanylate cyclase to chemotactic peptides. Acidifying agents inhibit motility, while artificial alkalization with ammonium chloride activates motility without egg factors. Thus increased internal pH, not decreased pH or mere external pH change without internal effect, initiates forward motility and chemosensory competence.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 7: Sperm activation via intracellular pH increase and Na+/H+ exchange.

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Sea urchin -l

Sperm motility in sea urchins is initiated by:

Uncapacitated sea urchin sperm stored within gonads maintains quiescent low-motility state due to relatively acidic intracellular pH around 7.2 and suppressed metabolism. Upon spawning into normal seawater pH approximately 8.0, Na+/H+ exchanger sNHE encoded by SLC9C1 extrudes protons raising internal pH to about 7.6, directly stimulating dynein ATPase activity, adenylate cyclase and flagellar beating. Intracellular pH elevation, potentiated further by resact-induced transient K+ efflux and hyperpolarization that activates sNHE, unlocks flagellar wave propagation. Artificially holding internal pH acidic even with abundant ATP prevents motility. Therefore increased internal pH initiates sperm motility and primes chemotaxis.

Ref: Lee et al., Dev Biol 1983, pH-dependent motility initiation; Gilbert Chapter 7: Sperm activation mechanisms.

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Fertilization in mammals-l

Main structural component of sperm flagellum:

Mammalian sperm flagellum core structure comprises microtubule-based axoneme anchored at basal body in neck region extending through midpiece and principal piece. Axoneme follows canonical 9+2 arrangement of nine doublet microtubules surrounding central pair, with outer dynein arms hydrolyzing ATP generating sliding between doublets converted to bending by radial spokes and nexin links. Accessory outer dense fibers and fibrous sheath provide elasticity. Microtubule dynamics drive progressive and hyperactivated motility; defects in axonemal components cause immotile cilia syndromes, primary ciliary dyskinesia, infertility due to impaired propulsion and flagellar function and reduced fertilization rates.

Ref: Fawcett, The Cell, 2nd ed., Chapter 15: 9+2 microtubule axoneme – dynein-driven motility of sperm flagellum.

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Fertilization in mammals-ll

Sperm hyperactivation is mediated by opening of:

Hyperactivation is vigorous, high-amplitude asymmetric flagellar beating pattern required for penetrating cumulus matrix and zona pellucida. Transition from progressive motility depends on massive calcium influx through sperm-specific CatSper complex located in principal piece of flagellum. Progesterone from cumulus and intracellular alkalinization during capacitation activate CatSper, raising flagellar calcium, stimulating calmodulin kinases and altering dynein motor regulation. Resultant whip-like thrust generates increased force, and pharmacologic CatSper blockade prevents hyperactivation demonstrating absolute channel dependence for fertilization competence and ascending oviductal transport mechanisms.

Ref: NCBI Bookshelf, Molecular Biology of the Cell, Chapter 15: CatSper and calcium-dependent hyperactivated motility mechanisms.

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