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首页> 外文期刊>International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience >Androgenic regulation of sexually dimorphic expression of RNA binding motif protein 48 in the developing mouse cortex and hippocampus
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Androgenic regulation of sexually dimorphic expression of RNA binding motif protein 48 in the developing mouse cortex and hippocampus

机译：雄激素调节在培养小鼠皮质和海马中RNA结合基序蛋白48中性三晶表达的调节

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摘要

To further reveal the molecular mechanism underlying sexual differentiation of the mouse cerebral cortex and hippocampus, we reanalyzed our previous microarray study with Gene Ontology (GO) term enrichment and found that the GO term "RNA binding" was over-represented among the 89 sexually dimorphic candidate genes. Thus, we selected 16 autosomal genes annotated to the term RNA binding and profiled their mRNA expression in the developing male and female mouse cortex/hippocampus. During the first three weeks after birth, sex differences in mRNA levels of Khdrbs2, Nanos2, Rbm48, and Tdrd3 were observed in the mouse cortex/hippocampus. Of these genes, only the female-biased expression of Rbm48 in neonates was abolished by prenatal exposure to testosterone propionate (TP), while postnatal treatment of TP three weeks after birth increased Rbm48 and Tdrd3 mRNA levels in both sexes. Regardless of sex, the postnatal cortex/hippocampus also showed a marked increase in the content of androgen receptor (Ar) and estrogen receptor beta (Esr2), but a decrease in estrogen receptor a (Esr1) and aromatase (Cyp19a1), which might confer the different responses of Rbm48 to prenatal and postnatal TP. Our results suggest that androgen-regulated, sexually dimorphic Rbm48 expression might present a novel molecular mechanism by which perinatal androgens control development of sexual dimorphism in cortical and hippocampal structure and function.
机译：为了进一步揭示小鼠脑皮质和海马的性分化的分子机制，我们重新分析了我们以前的微阵列与基因本体学（GO）富集的富集，发现GO术语“RNA结合”在89个性尺寸中过于表示候选基因。因此，我们选择了16个常染色体基因注释到术语RNA结合和分解其在发育雄性和雌性小鼠皮质/海马中的mRNA表达。在出生后的前三周，在小鼠皮质/海马中观察到KHDRBS2，NANOS2，RBM48和TDRD3的MRNA水平的性差异。在这些基因中，通过产前暴露于睾酮丙酸酯（TP）仅仅取消了新生儿中RBM48的雌性偏置的表达，而在出生后三周的TP产后治疗增加了两性的TD3 mRNA水平。不管性，后期皮质/海马也显示出雄激素受体（AR）和雌激素受体β（ESR2）的含量显着增加，但可能会赋予雌激素受体A（ESR1）和芳香酶（CYM19A1）的降低RBM48对产前和产后TP的不同反应。我们的研究结果表明，雄激素调节，性二晶RBM48表达可能提出一种新的分子机制，围产期和海马结构中性二晶体的疾病控制发展和功能。

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