First Author | Emmer BT | Year | 2020 |
Journal | PLoS One | Volume | 15 |
Issue | 1 | Pages | e0227450 |
PubMed ID | 31978056 | Mgi Jnum | J:284050 |
Mgi Id | MGI:6389148 | Doi | 10.1371/journal.pone.0227450 |
Citation | Emmer BT, et al. (2020) Murine Surf4 is essential for early embryonic development. PLoS One 15(1):e0227450 |
abstractText | Newly synthesized proteins co-translationally inserted into the endoplasmic reticulum (ER) lumen may be recruited into anterograde transport vesicles by their association with specific cargo receptors. We recently identified a role for the cargo receptor SURF4 in facilitating the secretion of PCSK9 in cultured cells. To examine the function of SURF4 in vivo, we used CRISPR/Cas9-mediated gene editing to generate mice with germline loss-of-function mutations in Surf4. Heterozygous Surf4+/- mice exhibit grossly normal appearance, behavior, body weight, fecundity, and organ development, with no significant alterations in circulating plasma levels of PCSK9, apolipoprotein B, or total cholesterol, and a detectable accumulation of intrahepatic apoliprotein B. Homozygous Surf4-/- mice exhibit embryonic lethality, with complete loss of all Surf4-/- offspring between embryonic days 3.5 and 9.5. In contrast to the milder murine phenotypes associated with deficiency of known SURF4 cargoes, the embryonic lethality of Surf4-/- mice implies the existence of additional SURF4 cargoes or functions that are essential for murine early embryonic development. |