| Speaker: | Susan S. Suarez ( (Biomedical Sciences, Cornell University) | |||
| Title: | Hyperactivated motility in mammalian sperm. |
| Abstract: |
When mammalian sperm are first deposited in the female reproductive tract, their flagella beat symmetrically and they swim in a straight path. A small percentage of sperm manage to reach and enter the oviduct, where they are soon trapped by sticking to its mucosal epithelium, and are thus stored until shortly before ovulation. At that time, sperm hyperactivate, increasing the amplitude of the principal flagellar bend. This enables sperm to pull off of the oviductal epithelium and execute sharp turns to escape from mucosal pockets. Hyperactivation also enhances sperm penetration of viscoelastic substances, such as oviductal mucous secretions and the cumulus matrix of the egg mass. Finally, hyperactivation turns sperm towards the oocyte and enables them to penetrate its glycoprotein shell, the zona pellucida. Calcium signaling is responsible for increasing the flagellar bend amplitude on one side of the flagellum to produce the asymmetrical bending characteristic of hyperactivation. The initial calcium signal may originate from a calcium store in the redundant nuclear envelope at the base of the flagellum. Plasma membrane channels, particularly those encoded by CatSper genes, provide calcium to sustain hyperactivation. The calcium binds to calmodulin, which, in turn, activates a calmodulin kinase II to phosphorylate targets in the flagellar axoneme. The identities of the axonemal targets, as well as the initial signal for hyperactivation remain to be discovered. NSF MCB 0421855.
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