First Author | Adams EJ | Year | 2021 |
Journal | Sci Rep | Volume | 11 |
Issue | 1 | Pages | 21100 |
PubMed ID | 34702932 | Mgi Jnum | J:312428 |
Mgi Id | MGI:6788027 | Doi | 10.1038/s41598-021-00579-x |
Citation | Adams EJ, et al. (2021) Murine SEC24D can substitute functionally for SEC24C during embryonic development. Sci Rep 11(1):21100 |
abstractText | The COPII component SEC24 mediates the recruitment of transmembrane cargos or cargo adaptors into newly forming COPII vesicles on the ER membrane. Mammalian genomes encode four Sec24 paralogs (Sec24a-d), with two subfamilies based on sequence homology (SEC24A/B and C/D), though little is known about their comparative functions and cargo-specificities. Complete deficiency for Sec24d results in very early embryonic lethality in mice (before the 8 cell stage), with later embryonic lethality (E7.5) observed in Sec24c null mice. To test the potential overlap in function between SEC24C/D, we employed dual recombinase mediated cassette exchange to generate a Sec24c(c-d) allele, in which the C-terminal 90% of SEC24C has been replaced by SEC24D coding sequence. In contrast to the embryonic lethality at E7.5 of SEC24C-deficiency, Sec24c(c-d/c-d) pups survive to term, though dying shortly after birth. Sec24c(c-d/c-d) pups are smaller in size, but exhibit no other obvious developmental abnormality by pathologic evaluation. These results suggest that tissue-specific and/or stage-specific expression of the Sec24c/d genes rather than differences in cargo export function explain the early embryonic requirements for SEC24C and SEC24D. |