Expression pattern of STAT5A gene during early bovine embryogenesis

Growth hormone (GH) plays an important role in early embryo development. It has been shown to activate multiple pathways, the most comprehensively studied being the STAT/JAK (Signal transducers and activators of transcription/Janus kinase) pathway. The objective of the present study was to investigate STAT5A gene expression during early bovine embryogenesis. Real-time polymerase chain reaction (RT-PCR) was used to measure the abundance of STAT5A transcripts. The mRNA was present at all stages of preimplantation bovine embryos investigated. The most abundant STAT5A expression occurred at the 2-cell stage. Expression was markedly reduced between the 4-cell and 8-cell stages, coinciding with the known time of embryo genome activation and loss of maternal mRNAs. This finding suggests that the embryonic STAT5A gene is primarily activated by maternal gene products

Expression of PC, PCK1, PCK2, LDHB, FBP1 and G6PC genes in the liver of cows in the transition from pregnancy to lactation*

The effect of the transition of dairy cows from pregnancy to lactation on the expression of genes encoding enzymes involved in hepatic glucose metabolism was studied. Six Holstein-Friesian heifers were used for this study. Liver samples were collected by biopsy on day 7 before expected parturition (-7) and days 3 and 21 after parturition (+3 and +21, respectively). The mRNA levels of pyruvate carboxylase (PC), phosphoenolpyruvate carboxykinase 1 (PCK1), phosphoenolpyruvate carboxykinase 2 (PCK2), lactate dehydrogenase B (LDHB), fructose-1,6-bisphosphatase 1 (FBP1) and glucose-6-phosphatase (G6PC) were measured using quantitative real-time PCR. The expression of PC and PCK2 mRNA on day 3 of lactation was significantly higher than that on day 7 before parturition (P<0.05) and slightly higher than on day 21 postpartum. The LDHB gene showed the highest expression level on day 3 of lactation, as compared with day 7 prepartum (P<0.001) and day 21 postpartum (P<0.001). No differences were shown in PCK1, FBP1 and G6PC expression levels between pregnancy and early lactation

Maternal placenta modulates a deleterious fetal mutation

Intrauterine growth restriction (IUGR) is caused by dysregulation of placental metabolism. Paternally inherited IUGR mutations in the fetus influence maternal physiology via the placenta. However, it is not known whether the maternal placenta also affects the extent of IUGR in such fetuses. In cattle and other ruminants, maternal-fetal communication occurs primarily at the placentomes. We previously identified a 3 deletion in the noncoding MER1 repeat containing imprinted transcript 1 (MIMT1) gene that, when inherited from the sire, causes IUGR and late abortion in Ayshire cattle with variable levels of severity. Here, we compared the transcriptome and genomic imprinting in fetal and maternal placentome components of wild-type and MIMT1(Del/WT) fetuses before IUGR became apparent, to identify key early events. Transcriptome analysis revealed fewer differentially expressed genes in maternal than fetal MIMT1(Del/WT) placentome. AST1, within the PEG3 domain, was the only gene consistently reduced in IUGR in both fetal and maternal samples. Several genes showed an imprinting pattern associated with IUGR, of which only secernin 3 (SCRN3) and paternally expressed 3 (PEG3) were differentially imprinted in both placentome components. Loss of strictly monoallelic, allele-specific expression (similar to 80:20) of PEG3 in the maternal MIMT1(Del/WT) placenta could be associated with incomplete penetrance of MIMT1(Del). Our data show that dysregulation of the PEG3 domain is involved in IUGR, but also reveal that maternal placental tissues may affect the penetrance of the paternally inherited IUGR mutation.Peer reviewe