Laboratorio de Biología de la Reproducción, Departamento Biomédico, Facultad de Ciencias de la Salud, Universidad de Antofagasta, Antofagasta, Chile.
Department of Obstetrics, Gynecology and Women's Health, University of Missouri, Columbia, MO, USA.
Mol Hum Reprod. 2019 Oct 28;25(10):587-600. doi: 10.1093/molehr/gaz037.
One of the first events of mammalian sperm capacitation is the activation of the soluble adenyl cyclase/cAMP/protein kinase A (SACY/cAMP/PKA) pathway. Here, we evaluated whether the increase in PKA activity at the onset of human sperm capacitation is responsible for the activation of the sperm proteasome and whether this activation is required for capacitation progress. Viable human sperm were incubated with inhibitors of the SACY/cAMP/PKA pathway. The chymotrypsin-like activity of the sperm proteasome was evaluated using a fluorogenic substrate. Sperm capacitation status was evaluated using the chlortetracycline assay and tyrosine phosphorylation. To determine whether proteasomal subunits were phosphorylated by PKA, the proteasome was immunoprecipitated and tested on a western blot using an antibody against phosphorylated PKA substrates. Immunofluorescence microscopy analysis and co-immunoprecipitation (IPP) were used to investigate an association between the catalytic subunit alpha of PKA (PKA-Cα) and the proteasome. The chymotrypsin-like activity of the sperm proteasome significantly increased after 5 min of capacitation (P < 0.001) and remained high for the remaining incubation time. Treatment with H89, KT5720 or KH7 significantly decreased the chymotrypsin-like activity of the proteasome (P < 0.001). IPP experiments indicated that PKA inhibition significantly modified phosphorylation of proteasome subunits. In addition, PKA-Cα colocalized with the proteasome in the equatorial segment and in the connecting piece, and co-immunoprecipitated with the proteasome. This is the first demonstration of sperm proteasome activity being directly regulated by SACY/PKA-Cα. This novel discovery extends our current knowledge of sperm physiology and may be used to manage sperm capacitation during assisted reproductive technology procedures.
哺乳动物精子获能的第一个事件之一是激活可溶性腺苷酸环化酶/cAMP/蛋白激酶 A(SACY/cAMP/PKA)途径。在这里,我们评估了人精子获能起始时 PKA 活性的增加是否负责激活精子蛋白酶体,以及这种激活是否是获能进展所必需的。将有活力的人精子与 SACY/cAMP/PKA 途径的抑制剂一起孵育。使用荧光底物评估精子蛋白酶体的糜蛋白酶样活性。使用氯四环素测定法和酪氨酸磷酸化来评估精子获能状态。为了确定蛋白酶体亚基是否被 PKA 磷酸化,用针对磷酸化 PKA 底物的抗体对蛋白酶体进行免疫沉淀,并在 Western blot 上进行测试。免疫荧光显微镜分析和共免疫沉淀(IPP)用于研究 PKA 的催化亚基α(PKA-Cα)与蛋白酶体之间的关联。精子蛋白酶体的糜蛋白酶样活性在获能 5 分钟后显著增加(P < 0.001),并在剩余的孵育时间内保持较高水平。用 H89、KT5720 或 KH7 处理显著降低蛋白酶体的糜蛋白酶样活性(P < 0.001)。IPP 实验表明,PKA 抑制显著改变了蛋白酶体亚基的磷酸化。此外,PKA-Cα 在赤道段和连接段与蛋白酶体共定位,并与蛋白酶体共免疫沉淀。这是首次证明精子蛋白酶体活性直接受 SACY/PKA-Cα 调节。这一新颖的发现扩展了我们对精子生理学的现有认识,并可用于在辅助生殖技术过程中管理精子获能。