reproductive system
N |
• spermatogenesis proceeded normally, as indicated by the presence and production of mature sperm
• microscopy revealed that epididymal sperm from mutant males were similar in number, viability, morphology, and motility to sperm from wild-type males
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• homozygous mutant male mice either produced few small litters or were sterile; in contrast, homozygous mutant females appeared to be fertile
(J:69105)
• in vitro fertilization experiments revealed that insemination with mutant sperm resulted in significantly fewer eggs becoming activated and that the calcium transients associated with fertilization were absent or delayed
(J:69105)
(J:82910)
|
• mutant sperm exhibited normal capacitation events, but failed to exhibit the expected intracellular [Ca2+]i mobilization in response to ZP
• progesterone, another physiological inducer of the acrosome reaction, failed to induce sustained [Ca2+]i increases in mutant sperm, also resulting in partial inhibition of the acrosome reaction
• finally, assessment of store-operated channel (SOC) function using thapsigargin indicated that capacitative Ca2+ entry through SOC channels was severely impaired in mutant sperm
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• mutant sperm were unable to initiate the acrosome reaction, an exocytotic event required for fertilization and induced by interaction with the zona pellucida (ZP)
(J:69105)
• progesterone, another physiological inducer of the acrosome reaction, failed to induce sustained [Ca2+]i increases in mutant sperm, also resulting in partial inhibition of the acrosome reaction
(J:82910)
|