RT Journal Article
SR Electronic
T1 PEG10 viral aspartic protease domain is essential for the maintenance of fetal capillary structure in the mouse placenta
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.03.02.433660
DO 10.1101/2021.03.02.433660
A1 Hirosuke Shiura
A1 Ryuichi Ono
A1 Saori Tachibana
A1 Takashi Kohda
A1 Tomoko Kaneko-Ishino
A1 Fumitoshi Ishino
YR 2021
UL http://biorxiv.org/content/early/2021/03/02/2021.03.02.433660.abstract
AB The therian-specific gene paternally expressed 10 (Peg10) plays an essential role in placenta formation: Peg10 knockout (KO) mice exhibit early embryonic lethality due to severe placental defects. The PEG10 protein exhibits homology to long terminal repeat (LTR) retrotransposon GAG and POL proteins, therefore mice harboring a mutation in its highly conserved viral aspartic protease motif in the POL-like region were generated because it is essential for LTR retrotransposons/retroviruses. Intriguingly, frequent perinatal lethality, not early embryonic lethality, was observed with fetal and placental growth retardation starting mid-gestation. In the mutant placentas, severe defects were observed in the fetal vasculature, where PEG10 is expressed in the three trophoblast cell layers that surround fetal capillary endothelial cells. Thus, Peg10 has essential roles not only in early placenta formation, but also in placental vasculature maintenance from mid- to late-gestation. This implies that along the feto-maternal placenta interface an interaction occurs between two retrovirus-derived genes, Peg10 and retrotransposon Gag like 1 (Rtl1, also called Peg11), that is essential for the maintenance of fetal capillary endothelial cells.Summary statement Disruption of the highly conserved viral aspartic protease domain in PEG10 causes placental abnormality leading to perinatal lethality in mice.Competing Interest StatementThe authors have declared no competing interest.