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MicroRNAs01:22

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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns (non-coding regions of a gene) or intergenic regions (stretches of DNA present between genes). Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself, forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After the pre-miRNA...
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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Mismatch Repair01:20

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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A MicroRNA Linking Human Positive Selection and Metabolic Disorders.

Lifeng Wang1, Nasa Sinnott-Armstrong2, Alexandre Wagschal1

  • 1Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

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Summary

A microRNA (miR-128-1) at a key human genetic locus influences energy storage. Its regulation may explain ancient famine adaptation and modern metabolic diseases like obesity and type 2 diabetes.

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Area of Science:

  • Genetics
  • Metabolic Diseases
  • Evolutionary Biology

Background:

  • The 2q21.3 locus in Europeans shows positive selection, linked to lactase persistence for famine survival.
  • This locus is also associated with human obesity and type 2 diabetes, suggesting a dual role in adaptation and disease.

Purpose of the Study:

  • To investigate the role of microRNA-128-1 (miR-128-1), located within the 2q21.3 locus, as a regulator of mammalian metabolism.
  • To explore the connection between miR-128-1, energy storage, ancient famine adaptation, and modern metabolic maladaptation.

Main Methods:

  • Utilized antisense targeting and genetic ablation of miR-128-1 in mouse models of metabolic disease.
  • Assessed the impact of miR-128-1 manipulation on energy expenditure, diet-induced obesity, and glucose tolerance.

Main Results:

  • Genetic ablation or inhibition of miR-128-1 led to increased energy expenditure in mouse models.
  • These interventions ameliorated high-fat-diet-induced obesity and significantly improved glucose tolerance.

Conclusions:

  • miR-128-1 is identified as a critical metabolic regulator in mammals.
  • A 'thrifty phenotype' linked to miR-128-1-dependent energy storage may bridge evolutionary adaptation to famine with modern metabolic diseases due to nutritional excess.