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Proper compartmentalization of the sperm flagellum is essential for fertility. The annulus is a septin-based ring that demarcates the midpiece (MP) and the principal piece (PP). It is assembled at the flagellar base, migrates caudally, and halts upon arriving at the PP. However, the mechanisms governing annulus positioning remain unknown. We report that a Chibby3 (Cby3)/Cby1-interacting BAR domain-containing 1 (ciBAR1) complex is required for this process. Ablation of either gene in mice results in male fertility defects, caused by kinked sperm flagella with the annulus mispositioned in the PP. Cby3 and ciBAR1 interact and colocalize to the annulus near the curved membrane invagination at the flagellar pocket. In the absence of Cby3, periannular membranes appear to be deformed, allowing the annulus to migrate over the fibrous sheath into the PP. Collectively, our results suggest that the Cby3/ciBAR1 complex regulates local membrane properties to position the annulus at the MP/PP junction. [ABSTRACT FROM AUTHOR]

We found different genotypes for the complete hydatidiform mole (CHM), placenta and co-existing fetus derived from a single in vitro fertilized human oocyte by the analysis of short tandem repeat (STR) DNA markers. The molar tissue was found to be heterozygously androgenetic. The fetus and placenta contained identical maternal, but different paternal genomes. Two models were proposed to account for the identification of triple genetic identities in a single fertilized oocyte. In the first model, the oocyte was fertilized by a diploid sperm, resulting in diandric triploidy. Premature cytokinesis resulted in early splitting of a cytoplasmic fragment with one copy of the replicated sperm chromosome, which developed into a heterozygous CHM. The bipolar spindle in syngamy pulled the other copy of sperm chromosomes and replicated oocyte chromosomes to form two blastomeres, which develop into the fetus and placenta, respectively. In the second model, the oocyte was fertilized by two haploid sperms, followed by tripolar spindle formation. Whatever is the mechanism, this case provides direct evidence that CHM can be derived from an oocyte containing an intact maternal genome. [ABSTRACT FROM AUTHOR]

BACKGROUND Maternal hypothyroidism during pregnancy can cause adverse effects in the fetus. Scientific evidence has shown that probable thyroid-like function of some phthalates in vitro and in vivo, and phthalates exposure, can begin in utero. This study investigated the association between phthalate exposure and thyroid hormones in pregnant women. METHODS Serum and spot urine samples were collected from 76 Taiwanese pregnant women at second trimester. Thyroid hormones, including thyroid-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4) and free T4 (FT4) were analysed in serum samples, and five urinary phthalate monoesters, including mono butyl phthalate (MBP), monoethyl phthalate (MEP) and mono ethylhexyl phthalate (MEHP), were measured. RESULTS Urinary MBP, MEP and MEHP, the median levels of which were 81.8, 27.7 and 20.6 ng/ml, respectively, were the predominant substances in the urinary phthalate monoesters. Significant mild negative correlations were found between T4 and urinary MBP (R = −0.248, P 4 and urinary MBP (R = −0.368, P 4 and T4 (FT4: β = −0.110, P 4: β=−0.112, P = 0.003). CONCLUSIONS Exposure to di-n-butyl phthalate (DBP) may affect thyroid activity in pregnant women, but how DBP affects thyroid function is unclear. Further studies are needed to elucidate the mechanism of action and to investigate whether any other factors related to DBP exposure alter the thyroid function. [ABSTRACT FROM AUTHOR]

Human trophoblast invasion of decidualized endometrium is essential for placentation and is tightly regulated and involves trophoblast-decidual cell interaction. High temperature requirement A4 (HtrA4) is a secreted serine protease highly expressed in the invasive extravillous trophoblasts that invade decidua. In contrast, both HtrA1 and HtrA3 have been shown to inhibit trophoblast invasion. Here we provide evidence that decidua-secreted HtrA1 and HtrA3 antagonize HtrA4-mediated trophoblast invasion. We demonstrated that HtrA1 and HtrA3 interact with and degrade HtrA4 and thereby inhibit trophoblast- like JAR cell invasion. Specifically, HtrA1 and HtrA3 expression is up-regulated under decidualization conditions in endometrial stromal and epithelial cells, T-HESCs and Ishikawa cells, respectively. Conditioned media from these two cell lines after decidualization treatment suppress HtrA4-expressing JAR cell invasion in an HtrA1- or HtrA3-dependent manner. Co-culture of the HtrA4-expressing JAR cells with decidualization stimuli-treated T-HESC or Ishikawa monolayer also impairs JAR cell invasion, which can be reversed by HtrA1 or HtrA3 knockdown, supporting that HtrA1 and HtrA3 are crucial for trophoblast-decidual cell interaction in the control of trophoblast invasion. Our study reveals a novel regulatory mechanism of trophoblast invasion through physical and functional interaction between HtrA family members. [ABSTRACT FROM AUTHOR]

A prospective study was carried out to identify the association of the DAZL (deleted in azoospermia-like) gene with major semen parameters in 210 men with normal and 467 men with abnormal semen parameters. Primer extension analysis for single nucleotide polymorphisms (SNP) of DAZL and quantitative trait analysis on the association of allele/genotype frequencies, linkage disequilibrium characteristics and DAZL haplotypes with semen parameters were investigated. Of five SNP (260A←G, 386A←G, 520+34c←a, 584+28c←t and 796+36g←a) screened, 386A←G was significantly correlated with sperm count (P< 0.0001) and motility (P < 0.005) and 584+28c←t was marginally correlated with sperm morphology. After excluding 520+34c←a, which was not in the Hardy-Weinberg equilibrium, the major haplotypes consisted of four SNP. One haplotype (260A←G (major allele), 386A←G (major allele), 584+28c←t (minor allele) and 796+36g←a (major allele)) was significantly associated with sperm count (P = 0.003) and motility (P = 0.04). This study suggests DAZL may be involved in regulating sperm counts, motility and possibly morphology. [ABSTRACT FROM AUTHOR]