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Pregnancy Timeline by SemestersDevelopmental TimelineFertilizationFirst TrimesterSecond TrimesterThird TrimesterFirst Thin Layer of Skin AppearsEnd of Embryonic PeriodEnd of Embryonic PeriodFemale Reproductive SystemBeginning Cerebral HemispheresA Four Chambered HeartFirst Detectable Brain WavesThe Appearance of SomitesBasic Brain Structure in PlaceHeartbeat can be detectedHeartbeat can be detectedFinger and toe prints appearFinger and toe prints appearFetal sexual organs visibleBrown fat surrounds lymphatic systemBone marrow starts making blood cellsBone marrow starts making blood cellsInner Ear Bones HardenSensory brain waves begin to activateSensory brain waves begin to activateFetal liver is producing blood cellsBrain convolutions beginBrain convolutions beginImmune system beginningWhite fat begins to be madeHead may position into pelvisWhite fat begins to be madePeriod of rapid brain growthFull TermHead may position into pelvisImmune system beginningLungs begin to produce surfactant
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development


Fertility can hinge on sperm swimming conditions

Female enzymes are specific to each woman in quality, quantity and sometimes function. New research finds a woman's enzymes in utero can improve sperm's ability to swim through the uterus and up a fallopian tube to an egg. Every mammal's sperm must make this swim, and the easier the swim, the better the chance for success.

Washington State University (WSU) researcher, Wipawee Winuthayanon PhD, now finds that the uterus in female mice contains Esr1 (estrogen receptor a), made up of enzymes that can cut through the gel-forming proteins semenogelin and collagen which make up semen. Esr1 makes seminal fluid less gel-like and more watery, thus easier to swim through. Scientists previously thought semen was only broken down by enzymes produced from the prostate gland, including kallikrein-related peptidases (KLKs) and especially KLK3 (or prostate specific antigen).

Writing this week in the journal PLOS Genetics, Winuthayanon, an assistant professor in the WSU School of Molecular Biosciences, reports female mice also produce Esr1, using estrogen to boost production. The team of researchers identified that when a female mouse lacks the gene to produce Esr1, semen fails to liquefy into the watery consistency sperm can navigate through freely.

"Our studies provide the first evidence of how the interplay between semen and the female reproductive tract could impact fertility."

Wipawee Winuthayanon PhD, School of Molecular Biosciences, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA.

Her study highlights an underappreciated complication in the physical changes secretions play on fertility in both the male and female reproductive tracts. The research could lead to development of diagnostic tools for unexplained infertility and perhaps a non-invasive contraception technology.

"This information will advance research on semen liquefaction in the female reproductive tract, an area that has never been explored. And, it could lead to the development of diagnostic tools for unexplained infertility cases as well as non-invasive contraception technologies."

Wipawee Winuthayanon PhD

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 (Wnt7aCre/+;Esr1f/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 Wnt7aCre/+;Esr1f/f uteri, compared to the watery semen (liquefied) found in Esr1f/f controls. In addition, semenogelin and collagen were not degraded in Wnt7aCre/+;Esr1f/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 Wnt7aCre/+;Esr1f/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.

Other Authors
Winuthayanon's colleagues on the study are post-doctoral research associate Shuai Li, honors student Marleny Garcia and research assistant Rachel L. Gewiss.
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Apr 26, 2017   Fetal Timeline   Maternal Timeline   News   News Archive   

Recent research finds human sperm need enzymes, from both father and mother, to break
down the gel-like proteins in semen surrounding sperm — allowing sperm to swim freely.
Image Credit: Avance Mundial


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