Summary BHCS3014 Capacitation, fertilisation and implantation
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Course
BHCS3014 Reproductive Sciences (BHCS3014)
Institution
Plymouth University (UOP)
Compiled from lecture notes, this is a condense but detailed summary of the the process of capacitation, fertilisation and implantation, studied within BHCS3014. Containing an overview of all the content in a logical order, easy to search and use for revision.
Capacitation
• Involves several biochemical and physiological changes in the sperm occurring in the female
reproductive tract prior to the acrosome reaction – fertilisation cannot occur without it
• Results in sperm having hyperactive motility
• Sperm swim up through cervix and uterus to reach ovulated secondary oocyte – sperm travels 30-
40cm
• Oocyte is only viable for 12-24 hours after ovulation; In female reproductive tract, sperm viable for
12-48 hours but some persist for 72 hours – therefore intercourse must occur 72 hour before and
24 hours after ovulation to maximise change of conceiving
• Glycoprotein must be removed – make sperm hyper-motile (cholesterol stabilises sperm
membrane after coat removed)
• Sperm ejaculation involves contractions of vas deferens mediated partly by P2X receptors (ligand-
gated cation channels)
• In female, sperm move to uterine tubes where they slow down and undergo capacitation
• Capacitation increase motility and prepares for acrosome reaction
• PI3K phosphorylated via PKA-dependent cascade and is downregulated by PKC
• PKC active at the beginning of capacitation = PI3K inactive
• During capacitation, PKC and PP12 are degraded by PKA-dependant mechanism, allowing PI3K
activation
• Activation of PI3K depend on cAMP (produced by adenylyl cyclase)
• PKA activation = actin polymerisation - essential process for development of hyperactivated
motility, necessary for successful fertilisation
• Actin
o Contractile protein
o Actin filaments (monomers) polymerised into a unit which is more effective that single thin
filaments
o More actin polymerisation = better swimmers
o G-actin = monomers; F-actin = actin polymer
o Actin polymerisation mediated by PIP2 in 2 ways
▪ PIP2 (2nd messenger) acts as co-factor for phospholipase D activation
▪ PIP2 binds and inhibits actin-severing protein gelsolin
o Ca and HCO3- influx to sperm causes PKA to inhibit gelsolin (as well as PIP 2) and stabilise
2+
polymerised actin (F-actin)
o When glycoprotein coat is lost, less cholesterol (efflux) in sperm membrane increase
permeability to Ca2+ and HCO3- = hyperactive motility (F-actin)
• Slow event – sperm motility activation
• Fast events
o Increase in tyrosine phosphorylation
o Hyperactivated sperm motility
o Preparation for acrosome reaction (losing coat)
Fertilisation
• Final stage of capacitation for acrosomal reaction to occur
o Ca2+ and cAMP dependant
o Acrosome is lysosome-like Golgi self-contained in sperm head
o Actin depolymerisation allows acrosome enzyme release
o Binding to ZP3 = Ca2+ influx through gated-channels (membrane depolarisation) → efflux of
Ca2+ from internal stores in cytosol = Ca2+ channels opening in plasma membrane =
acrosome reaction
• Acrosomal reaction
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