Abstract
Estrogen (E) plays a pivotal role in regulating the female reproductive system, particularly the ovary. However, the number and type of ovarian genes influenced by estrogen remain to be fully elucidated. In this study, we have utilized wild-type (WT) and aromatase knockout (ArKO; estrogen free) mouse ovaries as an in vivo model to profile estrogen dependent genes. RNA from each individual ovary (n = 3) was analyzed by a microarray-based screen using Illumina Sentrix Mouse WG-6 BeadChip (45,281 transcripts). Comparative analysis (GeneSpring) showed differential expression profiles of 450 genes influenced by E, with 291 genes up-regulated and 159 down-regulated by 2-fold or greater in the ArKO ovary compared to WT. Genes previously reported to be E regulated in ArKO ovaries were confirmed, in addition to novel genes not previously reported to be expressed or regulated by E in the ovary. Of genes involved in 5 diverse functional processes (hormonal processes, reproduction, sex differentiation and determination, apoptosis and cellular processes) 78 had estrogen-responsive elements (ERE). These analyses define the transcriptome regulated by E in the mouse ovary. Further analysis and investigation will increase our knowledge pertaining to how E influences follicular development and other ovarian functions.
Highlights
The importance of estrogen (E) in female reproductive endocrinology and in ovarian function has been well documented [1]
E-dependent Differentially expressed genes (DEG) in aromatase knockout (ArKO) compared to WTs
Microarray analysis of whole genome expression in ArKO ovary compared to WT ovary identified 450 differentially expressed transcripts with a 62-fold expression difference that was significant (p,0.05 according to t-tests, n = 3) (Table 1)
Summary
The importance of estrogen (E) in female reproductive endocrinology and in ovarian function has been well documented [1]. Estrogen signalling is primarily transduced by estrogen receptors (ER) a and b [2]. ER are members of a conserved superfamily of ligand activated transcription factors. The effects of E on ER are exerted through a complex array of convergent and divergent signaling pathways that mediate genomic events involved in regulation of mitogenesis, differentiation and apoptosis [3,4]. The interaction of E and ER with specific DNA sequences called estrogen responsive elements (EREs), constitutes a primary genomic signaling pathway [3,4]. The ERE-bound ER recruits an ensemble of co-factors responsible for the alteration of local chromatin structure and interaction with the basal transcription machinery
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