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Related Concept Videos

Animal Mitochondrial Genetics02:59

Animal Mitochondrial Genetics

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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Mitochondria01:37

Mitochondria

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Mitochondrial Membranes01:45

Mitochondrial Membranes

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A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
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Translocation of Proteins into the Mitochondria01:19

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Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
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Mitochondrial Precursor Proteins01:39

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Mitochondrial precursors are partially unfolded or loosely folded polypeptide chains. Newly synthesized precursors are inhibited from spontaneously folding into their native conformation by the cytosolic chaperones, heat shock proteins 70 (Hsp70), and mitochondrial import stimulation factors (MSFs). Precursors bound to MSFs are guided to the TOM70-TOM37 receptors, while precursors bound to Hsp70  chaperones are targetted to TOM20-TOM22 receptor complexes.
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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Author Spotlight: Decoding Mitochondrial Aging
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An evolutionary, or "Mitocentric" perspective on cellular function and disease.

Jamelle A Brown1, Melissa J Sammy2, Scott W Ballinger1

  • 1Department of Pathology, Division of Molecular and Cellular Pathology, University of Alabama at Birmingham, Birmingham, AL, 35294, USA.

Redox Biology
|June 9, 2020
PubMed
Summary
This summary is machine-generated.

Mito-Mendelian genetics, involving interactions between mitochondrial and nuclear DNA, may explain complex metabolic diseases. This new paradigm considers co-evolution of genomes influencing cell function and disease risk.

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Area of Science:

  • Genetics
  • Metabolic Diseases
  • Cell Biology

Background:

  • Complex metabolic diseases like obesity, cardiovascular disease, and diabetes are increasing globally.
  • Current genetic models struggle to explain the polygenic basis of these diseases.
  • The eukaryotic cell's origin involved symbiosis between mitochondrial and nuclear precursors.

Purpose of the Study:

  • To propose a new genetic paradigm, "mito-Mendelian genetics," for understanding complex disease etiology.
  • To investigate the role of genetic interaction and co-evolution between mitochondrial and nuclear genomes in disease risk.
  • To explore how natural variation in both genomes influences mitochondrial functions and disease development.

Main Methods:

  • Conceptual framework based on evolutionary history of eukaryotic cells.
  • Analysis of genetic interactions between mitochondrial and nuclear DNA.
  • Examination of co-evolutionary dynamics of these genomes.

Main Results:

  • Mito-Mendelian genetics offers a novel framework for complex disease research.
  • Genetic variation in both mitochondrial and nuclear DNA impacts mitochondrial functions.
  • Interplay between genomes influences energy production, cell signaling, and immune response.

Conclusions:

  • The co-evolution of mitochondrial and nuclear genomes is a significant factor in metabolic disease risk.
  • Mitochondrial metabolism, regulated by both genomes, is central to disease pathogenesis.
  • The mito-Mendelian genetics paradigm provides a new perspective on complex genetic diseases.