Dataset Information

Murine SEC24D can substitute functionally for SEC24C during embryonic development.

ABSTRACT: 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dual recombinase mediated cassette exchange to generate a Sec24c^c-d allele, in which the C-terminal 90% of SEC24C has been replaced by SEC24D coding sequence.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.

SUBMITTER: Adams EJ

PROVIDER: S-EPMC8548507 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature

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Murine SEC24D can substitute functionally for SEC24C during embryonic development.

Adams Elizabeth J EJ Khoriaty Rami R Kiseleva Anna A Cleuren Audrey C A ACA Tomberg Kärt K van der Ent Martijn A MA Gergics Peter P Tang Vi T VT Zhu Guojing G Hoenerhoff Mark J MJ O'Shea K Sue KS Saunders Thomas L TL Ginsburg David D

Scientific reports 20211026 1

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) ...[more]

PMID: 34702932

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Project description:IntroductionProlactin (PRL) is a pleiotropic hormone implicated in various physiological processes; however, its contribution to neurodevelopment, particularly early corticogenesis, remains insufficiently characterized. In this study, we investigate PRL's regulatory influence on the initial stages of cortical development, with an emphasis on its effects on neuronal and astrocytic differentiation.MethodsWe employed a standardized in vitro differentiation protocol to generate cortical neurons from mouse embryonic stem cells (mESCs). Prolactin receptor (PRLr) expression was evaluated in pluripotent stem cells, neural stem cells (NSCs), immature neurons, and mature neurons using both PCR and immunofluorescence. These analyses revealed dynamic changes in PRLr expression throughout the differentiation process. Additionally, cells were treated with varying concentrations of PRL during early and late differentiation phases, enabling assessment of its impact on neuronal phenotypic distribution and morphological complexity.ResultsEarly PRL administration significantly enhanced the population of β-tubulin III + immature neurons, promoting neuronal survival without altering NSC proliferation. Furthermore, PRL treatment increased the abundance of Tbr1 + and NeuN + neurons, augmented dendritic complexity, and accelerated neuronal maturation. In contrast, PRL exposure at later stages of neural differentiation did not yield comparable effects. Notably, PRL delayed the maturation of protoplasmic astrocytes, although the total astrocyte population was not affected.DiscussionThese findings highlight PRL's pivotal role as a regulator of early corticogenesis by modulating neuronal survival, dendritic development, and astrocyte maturation. PRL thus emerges as a potential key factor in neurodevelopment, underscoring its importance in the hormonal regulation of neural differentiation and maturation. These insights may have broader implications for understanding the molecular and cellular mechanisms underlying normal and pathological neurodevelopment.

Dataset Information

Murine SEC24D can substitute functionally for SEC24C during embryonic development.

Publications

Murine SEC24D can substitute functionally for SEC24C during embryonic development.

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