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Semen liquefaction changes semen from a gel-like to watery consistency and is required for sperm to gain mobility and swim to the fertilization site in the Fallopian tubes. Kallikrein-related peptidases 3 (KLK3) and other kallikrein-related peptidases from male prostate glands are responsible for semen liquefaction by cleaving gel-forming proteins (semenogelin and collagen). In a physiological context, the liquefaction process occurs within the female reproductive tract. How seminal proteins interact with the female reproductive environment is still largely unexplored. We previously reported that conditional genetic ablation of  Esr1  (estrogen receptor α) in the epithelial cells of the female reproductive tract ( Wnt7a  Cre/+ ; Esr1  f/f ) causes female infertility, partly due to a drastic reduction in the number of motile sperm entering the oviduct. In this study, we found that post-ejaculated semen from fertile wild-type males was solidified and the sperm were entrapped in  Wnt7a  Cre/+ ; Esr1  f/f  uteri, compared to the watery semen (liquefied) found in  Esr1  f/f  controls. In addition, semenogelin and collagen were not degraded in  Wnt7a  Cre/+ ; Esr1  f/f  uteri. Amongst multiple gene families aberrantly expressed in the absence of epithelial ESR1, we have identified that a lack of  Klks  in the uterus is a potential cause for the liquefaction defect. Pharmacological inhibition of KLKs in the uterus replicated the phenotype observed in  Wnt7a  Cre/+ ; Esr1  f/f  uteri, suggesting that loss of uterine and seminal KLK function causes this liquefaction defect. In human cervical cell culture, expression of several  KLKs  and their inhibitors ( SPINKs ) was regulated by estrogen in an ESR1-dependent manner. Our study demonstrates that estrogen/ESR1 signaling in the female reproductive tract plays an indispensable role in normal semen liquefaction, providing fundamental evidence that exposure of post-ejaculated semen to the suboptimal microenvironment in the female reproductive tract leads to faulty liquefaction and subsequently causes a fertility defect.

Crucial role of estrogen for the mammalian female in regulating semen coagulation and liquefaction in vivo