Psg22 null mouse embryos develop normally under normoxic and hypoxic conditions of pregnancy     

Abstract

Pregnancy-specific glycoproteins are secreted by immunoglobulin superfamily members encoded by multigene families in eutherian mammals with haemochorial placentation. They are expressed predominantly in placental trophoblast and exhibit immunomodulatory, anti-platelet, and pro-angiogenic functions. An inversion of Psg22 in the mouse locus is associated with relatively high Psg22 expression in the first half of the pregnancy. Bioinformatic analyses of 17 mouse strains indicated that Psg22 inversion arose at least 1.7 MYA. We used CRISPR-Cas9 mutagenesis to generate Psg22-null mutants, two of which were analysed in detail (Psg22 Δ10 and Psg22 Δ16). Both mutants contain frame-shifting deletions in exon 2, resulting in premature stop codons, and Psg22 mRNA was virtually undetectable. Both mutants are fertile and there was no distortion of Mendelian ratios in heterozygous crosses. Housing of pregnant females in a hypoxic (11% O 2) environment for 5 (E5-E10) or 10 (E5-E15) days did not induce differential growth or survival of Psg22 wildtype and null mutant genotypes. Our results indicate that Psg22 is dispensable for embryonic development and reproduction under laboratory conditions. As PSGs are secreted into maternal blood, future work will focus on whether Psg22 deficiency alters maternal physiology.