CatSper1 required for evoked Ca2+ entry and control of flagellar function in sperm

被引:320
作者
Carlson, AE
Westenbroek, RE
Quill, T
Ren, DJ
Clapham, DE
Hille, B
Garbers, DL
Babcock, DF
机构
[1] Univ Washington, Dept Physiol & Biophys, Seattle, WA 98195 USA
[2] Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA
[3] Univ Texas, SW Med Ctr, Dept Pharmacol, Dallas, TX 75390 USA
[4] Univ Texas, SW Med Ctr, Cecil H & Ida Green Ctr Reprod Biol Sci, Dallas, TX 75390 USA
[5] Univ Texas, SW Med Ctr, Howard Hughes Med Inst, Dallas, TX 75390 USA
[6] Univ Penn, Dept Biol, Philadelphia, PA 19104 USA
[7] Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp, Boston, MA 02115 USA
关键词
D O I
10.1073/pnas.2536658100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 [理学]; 0710 [生物学]; 09 [农学];
摘要
CatSper family proteins are putative ion channels expressed exclusively in membranes of the sperm flagellum and required for male fertility. Here, we show that mouse CatSper1 is essential for depolarization-evoked Ca2+ entry and for hyperactivated movement, a key flagellar function. CatSper1 is not needed for other developmental landmarks, including regional distributions of Ca(V)1.2, Ca(V)2.2, and Ca(V)2.3 ion channel proteins, the cAMP-mediated activation of motility by HCO3-, and the protein phosphorylation cascade of sperm capacitation. We propose that CatSper1 functions as a voltage-gated Ca2+ channel that controls Ca2+ entry to mediate the hyperactivated motility needed late in the preparation of sperm for fertilization.
引用
收藏
页码:14864 / 14868
页数:5
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