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A novel mouse model overexpressing Nocturnin results in decreased fat mass in male mice
Author(s) -
Le Phuong T.,
Bornstein Sheila A.,
Motyl Katherine J.,
Tian Li,
Stubblefield Jeremy J.,
Hong HeeKyung,
Takahashi Joseph S.,
Green Carla B.,
Rosen Clifford J.,
Guntur Anyonya R.
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28623
Subject(s) - biology , transgene , genetically modified mouse , phosphatase , adipose tissue , messenger rna , mitochondrion , microbiology and biotechnology , in vivo , stromal cell , gene , endocrinology , phosphorylation , biochemistry , cancer research , genetics
Nocturnin (NOCT) belongs to the Mg 2+ dependent Exonucleases, Endonucleases, Phosphatase (EEP) family of enzymes that exhibit various functions in vitro and in vivo. NOCT is known to function as a deadenylase, cleaving poly‐A tails from mRNA (messenger RNA) transcripts. Previously, we reported a role for NOCT in regulating bone marrow stromal cell differentiation through its interactions with PPARγ. In this study, we characterized the skeletal and adipose tissue phenotype when we globally overexpressed Noct in vivo. After 12 weeks of Noct overexpression, transgenic male mice had lower fat mass compared to controls, with no significant differences in the skeleton. Based on the presence of a mitochondrial target sequence in NOCT, we determined that mouse NOCT protein localizes to the mitochondria; subsequently, we found that NOCT overexpression led to a significant increase in the preadipocytes ability to utilize oxidative phosphorylation for ATP (adenosine triphosphate) generation. In summary, the effects of NOCT on adipocytes are likely through its novel role as a mediator of mitochondrial function.