Gene Essential for Female Fertility in Mice

Lack of gene leads to abnormal development and function of their reproductive system

THURSDAY, Aug. 21 (HealthDay News) -- Female mice missing a protein in their reproductive system needed for gene regulation are infertile due to abnormal development and function of their reproductive tract, according to a report published online Aug. 14 in Endocrinology.

Xiaoman Hong, and colleagues from the University of Kansas Medical Center in Kansas City generated mice with the Dicer1 gene deleted specifically in the developing female reproductive tract. Dicer1 generates small non-coding RNAs known as microRNAs that regulate gene expression post-transcriptionally, they note.

The researchers found that the mice displayed normal mating behavior but were unable to produce offspring with fertile males. Fertilization was successful and the fertilized eggs could develop normally to blastocysts in culture, but day 3 embryos were developmentally delayed compared with controls. Embryos also failed to enter the uterus on day 4 of pregnancy, suggesting a defect in oviductal transport. The uterus and oviduct of immature and adult female mice were hypotrophic and the oviduct was highly disorganized, according to the authors.

"These studies implicate Dicer1/microRNA mediated post-transcriptional gene regulation in reproductive somatic tissues as critical for the normal development and function of these tissues and for female fertility," Hong and colleagues conclude.

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