A key regulator of female fertility identified – potential as a target in fertility treatment
Within the sophisticated signalling network controlling female fertility, follicle-stimulating hormone (FSH), a keystone of fertility treatments, is critical to the development of mature eggs. FSH also self-regulates, stimulating the production of proteins, aptly named inhibins, that suppress its synthesis by the pituitary gland. Inhibin A targets a receptor called betaglycan, but researchers have only just identified a receptor for inhibin B, known as TGFBR3L. Female mice lacking TGFBR3L have slightly elevated FSH levels and larger litters, suggesting that, without TGFBR3L, inhibin B has less impact, and fertility increases. Yet, when both betaglycan and TGFBR3L are lost from pituitary gland cells, females display even higher FSH levels and much larger ovaries (pictured, right) compared to those lacking only TGFBR3L (left), and these mice are infertile. Understanding the different mechanisms underlying each FSH inhibitory pathway and especially the subtler effects of manipulating only TGFBR3L could suggest novel approaches to tackling infertility.
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