The mitochondrial‐derived peptide MOTS‐c: a player in exceptional longevity?

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Summary

Mitochondrial‐derived peptides ( MDP) are encoded by functional short open reading frames in the mitochondrial DNA (mt DNA). These include humanin, and the recently discovered mitochondrial open reading frame of the 12S rRNA‐c ( MOTS‐c). Although more research is needed, we suggest that the m.1382A>C polymorphism located in the MOTS‐c encoding mt DNA, which is specific for the Northeast Asian population, may be among the putative biological mechanisms explaining the high longevity of Japanese people.

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Most cited references 16

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The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.

Changhan Lee, Jennifer Zeng, Brian G. Drew … (2015)

Mitochondria are known to be functional organelles, but their role as a signaling unit is increasingly being appreciated. The identification of a short open reading frame (sORF) in the mitochondrial DNA (mtDNA) that encodes a signaling peptide, humanin, suggests the possible existence of additional sORFs in the mtDNA. Here we report a sORF within the mitochondrial 12S rRNA encoding a 16-amino-acid peptide named MOTS-c (mitochondrial open reading frame of the 12S rRNA-c) that regulates insulin sensitivity and metabolic homeostasis. Its primary target organ appears to be the skeletal muscle, and its cellular actions inhibit the folate cycle and its tethered de novo purine biosynthesis, leading to AMPK activation. MOTS-c treatment in mice prevented age-dependent and high-fat-diet-induced insulin resistance, as well as diet-induced obesity. These results suggest that mitochondria may actively regulate metabolic homeostasis at the cellular and organismal level via peptides encoded within their genome.

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A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta.

I Nishimoto, Y. Ito, Y Hashimoto … (2001)

Through functional expression screening, we identified a gene, designated Humanin (HN) cDNA, which encodes a short polypeptide and abolishes death of neuronal cells caused by multiple different types of familial Alzheimer's disease genes and by Abeta amyloid, without effect on death by Q79 or superoxide dismutase-1 mutants. Transfected HN cDNA was transcribed to the corresponding polypeptide and then was secreted into the cultured medium. The rescue action clearly depended on the primary structure of HN. This polypeptide would serve as a molecular clue for the development of new therapeutics for Alzheimer's disease targeting neuroprotection.

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Health span approximates life span among many supercentenarians: compression of morbidity at the approximate limit of life span.

S L Andersen, P Sebastiani, D. A. Dworkis … (2012)

We analyze the relationship between age of survival, morbidity, and disability among centenarians (age 100-104 years), semisupercentenarians (age 105-109 years), and supercentenarians (age 110-119 years). One hundred and four supercentenarians, 430 semisupercentenarians, 884 centenarians, 343 nonagenarians, and 436 controls were prospectively followed for an average of 3 years (range 0-13 years). The older the age group, generally, the later the onset of diseases, such as cancer, cardiovascular disease, dementia, and stroke, as well as of cognitive and functional decline. The hazard ratios for these individual diseases became progressively less with older and older age, and the relative period of time spent with disease was lower with increasing age group. We observed a progressive delay in the age of onset of physical and cognitive function impairment, age-related diseases, and overall morbidity with increasing age. As the limit of human life span was effectively approached with supercentenarians, compression of morbidity was generally observed.

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Author and article information

Journal

Journal ID (nlm-ta): Aging Cell

Journal ID (iso-abbrev): Aging Cell

Journal ID (doi): 10.1111/(ISSN)1474-9726

Journal ID (publisher-id): ACEL

Title: Aging Cell

Publisher: John Wiley and Sons Inc. (Hoboken )

ISSN (Print): 1474-9718

ISSN (Electronic): 1474-9726

Publication date (Electronic): 20 August 2015

Publication date (Print): December 2015

Volume: 14

Issue: 6 ( doiID: 10.1111/acel.2015.14.issue-6 )

Pages: 921-923

Affiliations

[ ¹ ] Graduate School of Health and Sports ScienceJuntendo University ChibaJapan

[ ² ]European University of Madrid MadridSpain

[ ³ ]Research Institute of Hospital 12 de Octubre (‘i+12’) MadridSpain

[ ⁴ ] Research Institute ‘Dr. Viña Giner’, Molecular and Mitochondrial MedicineCatholic University of Valencia San Vicente Mártir ValenciaSpain

[ ⁵ ] School of MedicineCatholic University of Valencia San Vicente Mártir ValenciaSpain

[ ⁶ ] Center for Supercentenarian StudyKeio University School of Medicine TokyoJapan

Author notes

[*] [* ] Correspondence

Alejandro Lucia, European University of Madrid, C/Tajo S/N, Urbanización El Bosque, Villaviciosa de Odón, Madrid, 28670 Spain. Tel .: (34) 916168265; fax: (34) 916168265; e‐mail: alejandro.lucia@ 123456uem.es

Article

Publisher ID: ACEL12389

DOI: 10.1111/acel.12389

PMC ID: 4693465

PubMed ID: 26289118

SO-VID: d32d0609-b050-4039-83f1-9eb9c0901609

License:

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

History

Date accepted : 21 July 2015

Page count

Pages: 3

Funding

Funded by: Grant‐in‐Aid for Scientific Research (B)

Award ID: 15H03081

Funded by: Ministry of Education, Culture, Sports, Science and Technology of Japan

Funded by: Fondo de Investigaciones Sanitarias

Award ID: PI12/00914

Funded by: Fondos FEDER

Custom metadata

source-schema-version-number 2.0

component-id acel12389

cover-date December 2015

details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.7.2 mode:remove_FC converted:22.12.2015

ScienceOpen disciplines: Cell biology

Keywords: aging,centenarians,longevity gene,longevity regulation,mitochondria,mitochondrial dna,mitochondrial dna abnormalities,molecular biology of aging

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ScienceOpen disciplines: Cell biology

Keywords: aging, centenarians, longevity gene, longevity regulation, mitochondria, mitochondrial dna, mitochondrial dna abnormalities, molecular biology of aging

The mitochondrial‐derived peptide MOTS‐c: a player in exceptional longevity?

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Most cited references 16

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.

A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta.

Health span approximates life span among many supercentenarians: compression of morbidity at the approximate limit of life span.

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