STUDIES OF SPERM FUNCTION IN MAMMALIAN FERTILIZATION

哺乳动物受精过程中精子功能的研究

• 批准号: 3312950
• 负责人: PATRICIA J OLDS-CLARKE
• 金额: $ 8.02万
• 依托单位: TEMPLE UNIV OF THE COMMONWEALTH
• 依托单位国家: 美国
• 财政年份: 1980
• 资助国家: 美国
• 起止时间: 1980-09-01 至 1990-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3312950
• 关键词: acidity /alkalinity; acrosome; calcium; cell membrane; chromosomes; developmental genetics; enzyme inhibitors; fertility promoting drug; fluorescent dye /probe; galactosyltransferases; gene mutation; genes; laboratory mouse; lactalbumin; sperm; sperm capacitation; sperm motility

The t complex in the mouse affects the function of sperm in fertilization. Sperm carrying a t complex (t sperm) from t/+ mice fertilize most or all oocytes. We have recently shown that this apparent advantage of t sperm in fertilization is due to the dysfunction of sperm not carrying a t complex (+ sperm) from the same male. The mechanism by which + sperm become defective, and the specific abnormalities which prevent them from participating in fertilization, are not known. We have shown that sperm from t/+ mice (mutant sperm), after several hours in vitro, develop a unique type of non-progressive motility called "dancing." We now have preliminary evidence that mutant sperm also begin hyperactivation (HA) sooner than sperm from congenic +/+ mice (normal sperm). Thus mutant sperm may have several motility defects. Our preliminary evidence indicates that the timing of capacitation (CAP) is similar in mutant and normal sperm, implying that HA occurs earlier than CAP in mutant sperm. If so, the t complex provides a unique system in which to study the relationship between HA and CAP. The overall objective of this proposal is to characterize the abnormalities in motility of mutant sperm, using the novel quantitative motility parameters we have developed to measure various aspects of translational (whole-sperm) movement in individual mouse sperm; to determine the relationship of the motility abnormalities to CAP; and to explore several approaches to investigating the mechanism(s) causing the abnormal motility. Specifically, we will determine the kinetics of HA, CAP and dancing in mutant sperm, and determine the factors upon which each of these processes is dependent. We will also probe the subcellular site of the cause of the defective motility and determine whether dancing or the early onset of HA is dependent on the other known defect of mutant sperm, elevated surface galactosyl transferase activity. The proposed studies will increase our understanding of how the t complex affects sperm motility, and how the t complex affects HA and CAP, sperm functions essential for fertilization. These studies may also provide clues to the cause of the abnormal motility. Since it appears that HA is uncoupled from CAP in mutant sperm, these experiments may also contribute to our knowledge of the relationship between HA and CAP in normal sperm.

小鼠中的T复合物会影响精子在 受精。 带有T/+小鼠的T复合物（T精子）的精子 施肥大多数或所有卵母细胞。 我们最近表明了这一点 T精子在受精方面的明显优势是由于 精子的功能障碍不会携带T复合物（+精子） 同一个男性。 +精子有缺陷的机制， 阻止他们参加的具体异常 在受精中，尚不清楚。 我们已经证明了T/+的精子 体外几个小时后，小鼠（突变精子）发展出独特的 非促进运动的类型称为“舞蹈”。 我们现在有 突变精子也开始过度激活的初步证据 （ha）比先生 +/ +小鼠的精子（正常精子）要早。 因此 突变精子可能有几个运动缺陷。 我们的初步 证据表明电容的时机（CAP）相似 在突变体和正常的精子中，这意味着HA的发生比 突变精子中的帽。 如果是这样，T综合体提供了独特的系统 在其中研究HA和CAP之间的关系。 该提议的总体目的是表征 使用小说的突变精子运动异常 我们开发的定量运动参数是为了测量 翻译（整个Sperm）运动的各个方面 单个小鼠精子；确定 上限运动异常；并探索几种方法 研究引起异常运动的机制。 具体而言，我们将确定HA，CAP和DANCEN的动力学 在突变的精子中，并确定每个因素的因素 过程取决于。 我们还将探测亚细胞位点 原因有缺陷的原因，并确定是否 跳舞或HA的早期发作取决于其他已知的 突变精子缺陷，表面半乳糖基转移酶升高 活动。 拟议的研究将提高我们对T的理解 复合物影响精子运动，T复合物如何影响HA 和CAP，精子功能对于受精至关重要。 这些 研究还可以提供异常原因的线索 运动。 由于似乎HA与突变体中的CAP未偶联 精子，这些实验也可能有助于我们了解 正常精子中的HA和CAP之间的关系。