Several families of endogenous retroviruses (ERVs) are expressed in mammalian placental tissues, and are implicated in aspects of placental development and function. We characterized the structure of abundant ERV-related transcripts in mouse placenta. In addition to the 7 kb full-length type I and 5 kb type I deleted intracisternal A-particle (IAP) transcripts, we identified and cloned an abundant 2 kb transcript encoding a novel member of the pregnancy-specific glycoprotein (Psg) gene family, which contains an IAP long terminal repeat (LTR) in the 3' untranslated region (UTR). The polyadenylation signal for the transcript is provided by the inserted LTR sequence. This sequence is allelic to Psg23 and is therefore denoted as Psg23(LTR). The transcript encodes a protein of 471 amino acids and has a domain organisation similar to previously described Psg proteins. Modelling of the protein N-domain produced a structure in good agreement with an existing crystalline structure for mouse sCEACAM1a. The LTR insertion is widely distributed among inbred mouse strains but is not found in 129/sv, CBA/2, or in wild mice. Cloning of the genomic region downstream of the LTR insertion site from the C57Bl/6J strain indicates that the insertion consists of a solo LTR without additional IAP sequence, and identified the original Psg23 polyadenylation signal sequence downstream of the insertion site. Psg23(LTR) was mapped to proximal chromosome 7 using the European collaborative interspecific mouse backcross (EUCIB) panel, and to yeast artificial chromosome (YAC) E072, which contains other members of the Psg gene family, by polymerase chain reaction (PCR). Northern blot analysis of RNA from adult and fetal mouse tissues and in situ hybridization to mid-gestation mouse embryos indicated that Psg23(LTR) is expressed predominantly in placental spongiotrophoblast. We detected a small, but statistically non-significant, bias in favour of transmission of Psg23(LTR) to the offspring of heterozygous parents. However, a larger study would be required to determine whether this allele is selectively advantageous to the developing embryo.
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http://dx.doi.org/10.1016/j.gene.2003.10.001 | DOI Listing |
Int J Mol Sci
January 2025
Department of Clinical Biochemistry, University Hospital Southampton NHS Foundation Trust, Southampton General Hospital, Southampton SO16 6YD, UK.
From fertilisation to delivery, calcium must be transported into and within the foetoplacental unit for intracellular signalling. This requires very rapid, precisely located Ca transfers. In addition, from around the eighth week of gestation, increasing amounts of calcium must be routed directly from maternal blood to the foetus for bone mineralisation through a flow-through system, which does not impact the intracellular Ca concentration.
View Article and Find Full Text PDFVet Rec
January 2025
Department of Obstetrics and Gynaecology, Faculty of Veterinary Medicine, Harran University, Sanliurfa, Turkey.
Background: This study aimed to evaluate the effects of administering flunixin meglumine (FM) and meloxicam (M) on specific days post-mating on progesterone (P4), total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), pregnancy-specific protein B (PSPB), pregnancy-associated glycoprotein (PAG) concentrations and fertility parameters in Awassi sheep.
Methods: Seventy-five Awassi sheep were divided into three groups of 25: control, M and FM. On days 9 and 10 post-mating, the control group received saline, the M group received 0.
Am J Perinatol
December 2024
Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland.
Development
November 2024
MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University Medical School, Nanjing 210093, China.
22q11.2 deletion syndrome (22q11.2DS) is the most common chromosomal microdeletion syndrome.
View Article and Find Full Text PDFbioRxiv
October 2024
John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL, USA.
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