Murine SEC24D can substitute functionally for SEC24C during embryonic development

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 abo...

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Bibliographic Details
Published in:Scientific reports 2021-10, Vol.11 (1), p.21100-21100, Article 21100
Main Authors: Adams, Elizabeth J., Khoriaty, Rami, Kiseleva, Anna, Cleuren, Audrey C. A., Tomberg, Kärt, van der Ent, Martijn A., Gergics, Peter, Tang, Vi T., Zhu, Guojing, Hoenerhoff, Mark J., O’Shea, K. Sue, Saunders, Thomas L., Ginsburg, David
Format: Article
Language:English
Subjects:
631/80/313/1463
631/80/313/2379
Animals
Cloning
Embryogenesis
Embryonic Development
Embryonic growth stage
Gene expression
Genetic Complementation Test
Genomes
Homology
Humanities and Social Sciences
Juveniles
Laboratory animals
Lethality
Membrane vesicles
Mice
Mice, Transgenic
multidisciplinary
Proteins
Recombinase
Science
Science (multidisciplinary)
Vesicular Transport Proteins - biosynthesis
Vesicular Transport Proteins - genetics
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Summary: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dual recombinase mediated cassette exchange to generate a Sec24c c-d allele, in which the C-terminal 90% of SEC24C has been replaced by SEC24D coding sequence.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.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-021-00579-x