scholarly journals Studies on Mitochondrial Structure and Function in Physarum polycephalum. VIII. Distribution of Mitochondrial DNA Molecules during Mitochondria Division

1979 ◽  
Vol 4 (2) ◽  
pp. 99-108 ◽  
Author(s):  
Shigeyuki Kawano ◽  
Tsuneyoshi Kuroiwa
Keyword(s):  
Mitochondrial Dna ◽  
Physarum Polycephalum ◽  
Structure And Function ◽  
Dna Molecules ◽  
Mitochondrial Structure ◽  
And Function

scholarly journals Studies on mitochondrial structure and function in Physarum polycephalum. V. Behaviour of mitochondrial nucleoids throughout mitochondrial division cycle.

1977 ◽  
Vol 72 (3) ◽  
pp. 687-694 ◽  
Author(s):  
T Kuroiwa ◽  
S Kawano ◽  
M Hizume
Keyword(s):  
Physarum Polycephalum ◽  
Mitochondrial Membrane ◽  
Light And Electron Microscopy ◽  
Structure And Function ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Division ◽  
Mitochondrial Structure ◽  
Mitochondrial Nucleoids ◽  
And Function ◽  
Narrow Bridge

The fine structure of mitochondria and mitochondrial nucleoids in exponentially growing Physarum polycephalum was studied at various periods throughout the mitochondrial division cycle by light and electron microscopy. The mitochondrial nucleoid elongates lingitudinally while the mitochondrion increases in size. When the nucleoid reaches a length of approximately 1.5 mum the mitochondrial membrane invaginates at the center of the mitochondrion and separates the mitochondrial contents. However, the nucleoid does not divide even when the mitochondrial sections are connected by a very narrow bridge. Just before division of the mitochondrion, the nucleoid divides by constriction of the limiting membrane of the dividing mitochondrion. After division, one end of the nucleoid appears to be associated with the inner mitochondrial membrane. The nucleoid then again becomes situated in the center of the mitochondrion before repeating these same processes.

scholarly journals Non-CpG methylation biases bisulphite PCR towards low or unmethylated mitochondrial DNA: recommendations for the field

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Margaret J Morris ◽  
Luke B Hesson ◽  
Neil A Youngson
Keyword(s):  
Mitochondrial Dna ◽  
Nuclear Genome ◽  
Structure And Function ◽  
Cpg Methylation ◽  
Published Data ◽  
Mitochondrial Structure ◽  
Multiple Copies ◽  
Methodological Considerations ◽  
And Function ◽  
Pcr Techniques

Abstract Mitochondrial DNA (mtDNA) is a circular genome of 16 kb that is present in multiple copies in mitochondria. mtDNA codes for genes that contribute to mitochondrial structure and function. A long-standing question has asked whether mtDNA is epigenetically regulated similarly to the nuclear genome. Recently published data suggest that unlike the nuclear genome where CpG methylation is the norm, mtDNA is methylated predominantly at non-CpG cytosines. This raises important methodological considerations for future investigations. In particular, existing bisulphite PCR techniques may be unsuitable due to primers being biased towards amplification from unmethylated mtDNA. Here, we describe how this may have led to previous studies underestimating the level of mtDNA methylation and reiterate methodological strategies for its accurate assessment.

scholarly journals Heterochronic Parabiosis: Old Blood Induces Changes in Mitochondrial Structure and Function of Young Mice

2020 ◽  
Author(s):  
Jenny L Gonzalez-Armenta ◽  
Ning Li ◽  
Rae-Ling Lee ◽  
Baisong Lu ◽  
Anthony J A Molina
Keyword(s):  
Mitochondrial Respiration ◽  
Complex I ◽  
Structure And Function ◽  
Muscle Performance ◽  
Mitochondrial Morphology ◽  
Positive Effects ◽  
Mitochondrial Structure ◽  
And Function ◽  
Old Mice ◽  
Young Mice

Abstract Heterochronic parabiosis models have been utilized to demonstrate the role of blood-borne circulating factors in systemic effects of aging. In previous studies, heterochronic parabiosis has shown positive effects across multiple tissues in old mice. More recently, a study demonstrated old blood had a more profound negative effect on muscle performance and neurogenesis of young mice. In this study, we used heterochronic parabiosis to test the hypothesis that circulating factors mediate mitochondrial bioenergetic decline, a well-established biological hallmark of aging. We examined mitochondrial morphology, expression of mitochondrial complexes, and mitochondrial respiration from skeletal muscle of mice connected as heterochronic pairs, as well as young and old isochronic controls. Our results indicate that young heterochronic mice had significantly lower total mitochondrial content and on average had significantly smaller mitochondria compared to young isochronic controls. Expression of complex IV followed a similar pattern: young heterochronic mice had a trend for lower expression compared to young isochronic controls. Additionally, respirometric analyses indicate that young heterochronic mice had significantly lower complex I, complex I + II, and maximal mitochondrial respiration and a trend for lower complex II-driven respiration compared to young isochronic controls. Interestingly, we did not observe significant improvements in old heterochronic mice compared to old isochronic controls, demonstrating the profound deleterious effects of circulating factors from old mice on mitochondrial structure and function. We also found no significant differences between the young and old heterochronic mice, demonstrating that circulating factors can be a driver of age-related differences in mitochondrial structure and function.

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