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Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review article (species not specified; no experimental subjects) discusses mitochondrial-derived peptides (MDPs) — Humanin (HN), MOTS-c, and SHLP1-6 — encoded by short open-reading frames in mitochondrial DNA, and their described roles in disease. The authors describe the genetic origin of each MDP, including which strand and rRNA gene encodes them, and the distinct mitochondrial start/stop codon usage involved. The review focuses on reported roles of MDPs in disease pathology including Type 1 diabetes, Type 2 diabetes, gestational diabetes, Alzheimer's disease, cardiovascular disease, prostate cancer, and macular degeneration, with emphasis on MDP regulation of Type 1, Type 2, and gestational diabetes, and discusses evolutionary pressures for conservation of MDP amino acid sequences.
Abstract
Mitochondrial-derived peptides (MDPs) are a novel class of bioactive microproteins encoded by short open-reading frames (sORF) in mitochondrial DNA (mtDNA). Currently, three types of MDPs have been identified: Humanin (HN), MOTS-c (Mitochondrial ORF within Twelve S rRNA type-c), and SHLP1-6 (small Humanin-like peptide, 1 to 6). The 12 S ribosomal RNA (MT-RNR1) gene harbors the sequence for MOTS-c, whereas HN and SHLP1-6 are encoded by the 16 S ribosomal RNA (MT-RNR2) gene. Special genetic codes are used in mtDNA as compared to nuclear DNA: (i) ATA and ATT are used as start codons in addition to the standard start codon ATG; (ii) AGA and AGG are used as stop codons instead of coding for arginine; (iii) the standard stop codon UGA is used to code for tryptophan. While HN, SHLP6, and MOTS-c are encoded by the H (heavy owing to high guanine + thymine base composition)-strand of the mtDNA, SHLP1-5 are encoded by the L (light owing to less guanine + thymine base composition)-strand. MDPs attenuate disease pathology including Type 1 diabetes (T1D), Type 2 diabetes (T2D), gestational diabetes, Alzheimer's disease (AD), cardiovascular diseases, prostate cancer, and macular degeneration. The current review will focus on the MDP regulation of T2D, T1D, and gestational diabetes along with an emphasis on the evolutionary pressures for conservation of the amino acid sequences of MDPs.
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