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

原始卵泡禀赋、BEL-2 和 BCL-X

• 批准号: 6387728
• 负责人: Jodi A. Flaws
• 金额: $ 24.55万
• 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 2004-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6387728
• 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