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Buffering brain development: sex-bias miRNA and gene expression
Graduate Thesis/Dissertation   Open access

Buffering brain development: sex-bias miRNA and gene expression

Rachel Jane Cannon
Master of Science - MSc, University of Otago
University of Otago
2024
Handle:
https://hdl.handle.net/10523/16638

Abstract

ESR1 ESR2 Estrogen Cell culture chromatin immunoprecipitation Autism Schizophrenia Attention deficit hyperactivity disorder ERα ERβ MiRNA mice E15.5 embryonic neurodevelopment sex differences
The development of the embryonic brain is a critical process, and neurodevelopment disorders, such as attention deficit hyperactivity disorder, autism, and schizophrenia, can arise due to dysregulation during neurodevelopment. However, the cause for these disorders and the generation of sex differences displayed between the disorders are still largely unknown research areas. Current theories of contribution towards sex differences generated in neurodevelopment disorders suggest the dysregulation of miRNAs, a small non-coding RNA essential for neurodevelopment that negatively regulates mRNA. A significant contribution to sex differences is hormones such as estrogen. An enzyme, aromatase, can convert testosterone to estrogen, and due to the early secretion of testosterone by the testis during development means that higher estrogen levels are found in males. Estrogen binds to the estrogen receptor, which can bind to gene regulatory elements to influence gene expression. Thereby, due to the role estrogen plays in the generation of sex and regulation, we suggest that estrogen has a role in regulating sex-biased miRNA gene expression. Here I have investigated the relationship between estrogen and miRNA in the embryonic wild-type E15.5 mouse brain by chromatin immunoprecipitation followed by Real-Time quantitative PCR. Potential regulatory DNA elements near seven miRNAs were investigated, and the results demonstrated sex differences in the recruitment of two estrogen receptors, Estrogen receptor 1 and Estrogen receptor 2. Recruitment of ERα was significant in the females, while ERβ bound significantly for the males for the miRNAs; miR-10b-5p, miR199a-5p, miR-200a-5p, miR-205-5p, and miR-206-3p. To further confirm if our investigated miRNAs were regulated by estrogen, E13.5 mice brain tissues were cultured and treated with β-estradiol. Four of the investigated miRNAs, miR10b-5p, miR-200c-3p, miR-205-5p, and miR-206-3p, showed significant responses following the addition of 17β-estradiol, and the response differed between the sexes. Females responded positively, while males responded negatively in addition to β-estradiol. This study provides further evidence for using different estrogen receptor types between the sexes and that for three investigated, miRNAs are regulated by estrogen. This provides evidence for a potential link between estrogen and miRNA gene regulation in the generation of sex differences during neurodevelopment.
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