<scp>SAMM</scp>50 Affects Mitochondrial Morphology through the Association of Drp1 in Mammalian Cells

Liu, Shuo; Gao, Yali; Zhang, Cheng; Li, Han; Pan, Shiyi; Wang, Xiaoli; Du, Shizheng; Deng, Zixin; Lian-rong, Wang; Song, Zhiyin; Chen, Shi

doi:10.1002/1873-3468.12170

Cited by 22 publications

(17 citation statements)

References 43 publications

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“…In the present study, we found that SAMM50 is widely expressed across different tissues in buffalo, especially in tissues with high level in energy metabolism such as the heart, liver, muscle, and adipose (Figure 3D). These results are consistent with its vital role in mitochondria (Liu et al, 2016;Jian et al, 2018). However, the effect of SAMM50 on adipogenic differentiation of adipocytes had not been revealed.…”

Section: Discussionsupporting

confidence: 76%

“…FABP4 is a significant protein in fatty acid transportation (Boord et al, 2002) and adipocyte differentiation (Garin-Shkolnik et al, 2014). SAMM50 is a mitochondrial membrane protein and is associated with energy metabolism in mammals (Liu et al, 2016). Considering the function of host genes and the lowest p value (Table 1), we focused on a lncRNA transcribed from the antisense strand of SAMM50, lncSAMM50.…”

Section: Discussionmentioning

confidence: 99%

“…The existing data suggest that lncRNA can play a role by regulating the expression of a host gene (Guo et al, 2019;Song et al, 2020), meaning that the function of a lncRNA is associated with its host gene. SAMM50 is the core component of the sorting and assembly machinery and plays a critical role in regulating mitochondrial dynamics and mitophagy (Liu et al, 2016;Jian et al, 2018), indicating a significant role of SAMM50 in energy metabolism. In the present study, we found that SAMM50 is widely expressed across different tissues in buffalo, especially in tissues with high level in energy metabolism such as the heart, liver, muscle, and adipose (Figure 3D).…”

Section: Discussionmentioning

confidence: 99%

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lncSAMM50 Enhances Adipogenic Differentiation of Buffalo Adipocytes With No Effect on Its Host Gene

et al. 2021

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Fat deposition is one of the most important traits that are mediated by a set of complex regulatory factors in meat animals. Several researches have revealed the significant role of long non-coding RNAs (lncRNAs) in fat deposition while the precise regulatory mechanism is still largely elusive. In this study, we investigated the lncRNA profiles of adipose and muscle tissues in buffalo by using the Illumina HiSeq 3000 platform. In total, 43,809 lncRNAs were finally identified based on the computer algorithm. A comparison analysis revealed 241 lncRNAs that are differentially expressed (DE) in adipose and muscle tissues. We focused on lncSAMM50, a DE lncRNA that has a high expression in adipose tissue. Sequence alignment showed that lncSAMM50 is transcribed from the antisense strand of the upstream region of sorting and assembly machinery component 50 homolog (SAMM50), a gene involved in the function of mitochondrion and is subsequently demonstrated to inhibit the adipogenic differentiation of 3T3-L1 adipocyte cells in this study. lncSAMM50 is highly expressed in adipose tissue and upregulated in the mature adipocytes and mainly exists in the nucleus. Gain-of-function experiments demonstrated that lncSAMM50 promotes the adipogenic differentiation by upregulating adipogenic markers but with no effect on its host gene SAMM50 in buffalo adipocytes. These results indicate that lncSAMM50 enhances fat deposition in buffalo and provide a new factor for the regulatory network of adipogenesis.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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lncSAMM50 Enhances Adipogenic Differentiation of Buffalo Adipocytes With No Effect on Its Host Gene

et al. 2021

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“…The picture has been recently further complicated by additional OMM proteins shown to also promote Drp1 recruitment, such as SAMM50, a component of the SAM complex, which inserts beta barrels in the OMM [ 141 ]. SAMM50 has been shown to interact with Drp1 and induce Drp1-dependent mitochondrial fission through an unknown mechanism [ 142 ]. Interestingly, SAMM50 could coordinate outer and inner membrane fission, as it also interacts with VDAC, a component of OMM/IMM contact sites and with the MINOS/MITOS complex in the IMM.…”

Section: New Insights Into Drp1-dependent Mitochondrial Fissionmentioning

confidence: 99%

The ever-growing complexity of the mitochondrial fission machinery

Pagliuso

Cossart

Stavru

2017

Cell. Mol. Life Sci.

151

118

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The mitochondrial network constantly changes and remodels its shape to face the cellular energy demand. In human cells, mitochondrial fusion is regulated by the large, evolutionarily conserved GTPases Mfn1 and Mfn2, which are embedded in the mitochondrial outer membrane, and by OPA1, embedded in the mitochondrial inner membrane. In contrast, the soluble dynamin-related GTPase Drp1 is recruited from the cytosol to mitochondria and is key to mitochondrial fission. A number of new players have been recently involved in Drp1-dependent mitochondrial fission, ranging from large cellular structures such as the ER and the cytoskeleton to the surprising involvement of the endocytic dynamin 2 in the terminal abscission step. Here we review the recent findings that have expanded the mechanistic model for the mitochondrial fission process in human cells and highlight open questions.Electronic supplementary materialThe online version of this article (doi:10.1007/s00018-017-2603-0) contains supplementary material, which is available to authorized users.

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“…Sam50, an important mitochondria outer membrane protein, encoded by the SAMM50 gene and involved in the regulation of mitophagy, mitochondrial morphology and removal of ROS [ 175 ]. Several SNPs were linked with NAFLD; however, the exact mechanism, leading to hepatic lipids accumulation and NAFLD progression was not known.…”

Section: Genetic Determinants Of the Nafld Pathogenesismentioning

confidence: 99%

Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk

Dabravolski

Bezsonov

Baig

et al. 2021

IJMS

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NAFLD (non-alcoholic fatty liver disease) is a widespread liver disease that is often linked with other life-threatening ailments (metabolic syndrome, insulin resistance, diabetes, cardiovascular disease, atherosclerosis, obesity, and others) and canprogress to more severe forms, such as NASH (non-alcoholic steatohepatitis), cirrhosis, and HCC (hepatocellular carcinoma). In this review, we summarized and analyzed data about single nucleotide polymorphism sites, identified in genes related to NAFLD development and progression. Additionally, the causative role of mitochondrial mutations and mitophagy malfunctions in NAFLD is discussed. The role of mitochondria-related metabolites of the urea cycle as a new non-invasive NAFLD biomarker is discussed. While mitochondria DNA mutations and SNPs (single nucleotide polymorphisms) canbe used as effective diagnostic markers and target for treatments, age and ethnic specificity should be taken into account.

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SAMM50 Affects Mitochondrial Morphology through the Association of Drp1 in Mammalian Cells

Cited by 22 publications

References 43 publications

lncSAMM50 Enhances Adipogenic Differentiation of Buffalo Adipocytes With No Effect on Its Host Gene

lncSAMM50 Enhances Adipogenic Differentiation of Buffalo Adipocytes With No Effect on Its Host Gene

The ever-growing complexity of the mitochondrial fission machinery

Mitochondrial Mutations and Genetic Factors Determining NAFLD Risk

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