THE PRIMORDIAL FOLLICLE ENDOWMENT, BEL-2 AND BCL-X

原始卵泡禀赋、BEL-2 和 BCL-X

• 批准号: 6637940
• 负责人: Jodi A. Flaws
• 金额: $ 23.46万
• 依托单位: UNIVERSITY OF MARYLAND BALTIMORE
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-07-01 至 2005-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6637940
• 关键词: BCL2 gene /protein; RNase protection assay; apoptosis; aromatic hydrocarbon receptor; cell growth regulation; cell proliferation; corpus luteum; cyclohexane /cyclohexene carboxylate; developmental genetics; disease /disorder model; embryogenesis; estrus; gene expression; gene induction /repression; genetic manipulation; genetically modified animals; germ cells; graafian follicles; histopathology; immunocytochemistry; laboratory mouse; oncoproteins; ovary disorder; protooncogene; tissue /cell culture

Little is known about how the size of the primordial follicle pool at birth affects the rates of follicular growth/atresia and the timing of the onset of estrous cyclicity in postnatal life. This application proposes to use several mouse models to test the hypotheses that: the number of primordial follicles at birth is determined by the number of germ cells present in embryonic life, and the initial size of the primordial follicle pool at birth affects the rate of follicular growth/atresia in the neonatal and prepubertal periods so that the number of primordial follicles at the onset of maturity have become normalized (returned to normal levels). The specific aims for this project are to determine whether (1) a genetically-induced excess of primordial follicles at birth is due to a surfeit of germ cells and/or somatic cells during embryonic life; and evaluate whether an above number of primordial follicles at birth increases the rates of follicular growth/atresia and the onset of cyclicity in postnatal life, (2) a genetically-induced deficiency of primordial follicles at birth is due to a deficiency of germ cells and/or somatic cells during embryonic life; and evaluate whether a below normal number of primordial follicles decreases the rates of follicular growth/atresia and the onset of cyclicity in postnatal life, (3) a chemically-induced deficiency of primordial follicles at birth affects the rates of follicular growth/atresia and delays the onset of cyclicity in postnatal life, and (4) the genetic and chemical manipulations affects primordial follicle numbers via common mechanisms. The results of the proposed studies will provide critical information about the embryonic factors that establish the size of the primordial follicle pool. It also will clarify how the size of the primordial follicle endowment affects the rates of follicular growth/atresia in postnatal life and the timing of the onset of puberty.

人们对原始卵泡池的大小知之甚少 出生时影响卵泡生长/闭锁的速度和出生的时间 发情周期在出生后的生活中开始。此应用程序建议使用 用几个小鼠模型来检验假设：原始数量 出生时的卵泡由体内存在的生殖细胞数量决定 胚胎寿命和出生时原始卵泡池的初始大小 影响新生儿和青春期前卵泡生长/闭锁的因素 成熟初期原始卵泡的数量 已经正常化(恢复到正常水平)。这方面的具体目标 项目是确定(1)基因诱导的原始细胞过剩 出生时的卵泡是由于生殖细胞和/或体细胞过多所致。 在胚胎生命期间；并评估是否有以上数量的原始 出生时的卵泡增加了卵泡生长/闭锁的比率和 在出生后生活中开始周期性，(2)遗传导致的 出生时的原始卵泡是由于生殖细胞和/或 胚胎生命中的体细胞；并评估是否有低于正常数量的 原始卵泡减少卵泡生长/闭锁率和 出生后生命周期的开始，(3)化学诱导的缺陷 出生时原始卵泡的数量影响卵泡生长/闭锁的速度 并延迟出生后生命的周期性的开始，以及(4)遗传和 化学操作通过共同作用影响原始卵泡数量 机制。拟议研究的结果将提供关键的 关于胚胎因素的信息，这些因素决定了 原始毛囊池。它还将阐明原始生物的大小是如何 卵泡发育状况对出生后卵泡生长/闭锁的影响 生命和青春期开始的时间。