| First Author | Carlini MJ | Year | 2024 |
| Journal | Biochem Biophys Res Commun | Volume | 712-713 |
| Pages | 149923 | PubMed ID | 38640735 |
| Mgi Jnum | J:347623 | Mgi Id | MGI:7625750 |
| Doi | 10.1016/j.bbrc.2024.149923 | Citation | Carlini MJ, et al. (2024) Stasimon/Tmem41b is required for cell proliferation and adult mouse survival. Biochem Biophys Res Commun 712-713:149923 |
| abstractText | Stasimon/Tmem41b is a transmembrane protein with phospholipid scrambling activity that resides in the endoplasmic reticulum and has been implicated in autophagy, lipid metabolism, and viral replication. Stasimon/Tmem41b has also been linked to the function of sensory-motor circuits and the pathogenesis of spinal muscular atrophy. However, the early embryonic lethality of constitutive knockout in mice has hindered the analysis of spatial and temporal requirements of Stasimon/Tmem41b in vivo. To address this, we developed a novel mouse line harboring a conditional knockout allele of the Stasimon/Tmem41b gene in which exon 4 has been flanked by loxP sites (Stas/Tmem41b(CKO)). Cre-mediated recombination of Stas/Tmem41b(CKO) generates a functionally null allele (Stas/Tmem41b(Delta4)) resulting in loss of protein expression and embryonic lethality in the homozygous mouse mutant. Here, using a ubiquitously expressed, tamoxifen inducible Cre recombinase in the homozygous Stas/Tmem41b(CKO) mice, we demonstrate that postnatal depletion of Stasimon/Tmem41b rapidly arrests weight gain in adult mice and causes motor dysfunction and death approximately three weeks after tamoxifen treatment. Moreover, we show that depletion of Stasimon/Tmem41b severely affects cell proliferation in mouse embryonic fibroblasts. This study provides new insights into the essential requirement of Stasimon/Tmem41b for cellular and organismal fitness and expands the experimental toolkit to investigate its functions in the mammalian system. |
