Studies on the mechanism of flagellar movement using mammalian seminal plasma motility inhibitor protein.

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Mammalian seminal plasma contains a inhibitor to immobilize the demembranated flagellar movement. The inhibitor (SPMI, seminal plasma motility inhibitor) was prepared from the boar. The purified SPMI was consisted with three subunits, 14, 16 and 18 KD in SDSPAGE. SPMI inhibited not only mammalian but also fish and sea urchin sperm flagellar movement so that it seemed to inhibit the flagellar movement universally. When the demembranated sea urchin sperm flagella were exposed to SPMI the amplitude of bend decreased apparently, followed by irregular beat and then, stopped. The sliding disintegration of doublet microtubules were inhibited by SPMI, however, the end of flagella split out to individual microtubules and the bends were relaxed. ATPase activity was partially inhibited by SPMI. It was assumed that the amplitude of flagellar bend was closely related to the viscoelasticity in flagellar axoneme and SPMI increased it. It was also observed that the very slow bend propagation occurred in the presence of high concentration of SPMI. In that case, some wave parameters were preserved during the bend propagation, suggesting that these parameters should be very important to understanding the control mechanism of flagellar movement.Effects of poly amino acid on flagellar movement was studied. Only the basic and high molecular weight (15 KD or more) poly amino acids such as poly-L-lysine (PLL) inhibited the flagellar movement. The bend amplitude rather than the beat frequency was inhibited by PLL. Bends were relaxed even in the presence of high concentration of PLL. These results suggested that the inhibition manner of PLL was similar to that of SPMI in some parts. Therefore, it was likely that PLL increased the inter microtubule viscoelasticity.The microinjection of SPMI into the sea urchin blastomere was carried out. SPMI provided some inhibitory effects in a certain period prior to the cell division.