scholarly journals Directed Mutations Recode Mitochondrial Genes: From Regular to Stopless Genetic Codes

2018 ◽  
Author(s):  
Hervé Seligmann
Keyword(s):  
Mitochondrial Genes ◽  
Genetic Codes

scholarly journals Improving Phylogenetic Signals of Mitochondrial Genes Using a New Method of Codon Degeneration

Life ◽  
2020 ◽  
Vol 10 (9) ◽  
pp. 171
Author(s):  
Xuhua Xia
Keyword(s):  
Rapid Evolution ◽  
Nucleotide Composition ◽  
Mitochondrial Genes ◽  
Phylogenetic Position ◽  
Standard Genetic Code ◽  
Nucleotide Level ◽  
Synonymous Codons ◽  
Genetic Codes ◽  
User Friendly ◽  
Phylogenetic Noise

Recovering deep phylogeny is challenging with animal mitochondrial genes because of their rapid evolution. Codon degeneration decreases the phylogenetic noise and bias by aiming to achieve two objectives: (1) alleviate the bias associated with nucleotide composition, which may lead to homoplasy and long-branch attraction, and (2) reduce differences in the phylogenetic results between nucleotide-based and amino acid (AA)-based analyses. The discrepancy between nucleotide-based analysis and AA-based analysis is partially caused by some synonymous codons that differ more from each other at the nucleotide level than from some nonsynonymous codons, e.g., Leu codon TTR in the standard genetic code is more similar to Phe codon TTY than to synonymous CTN codons. Thus, nucleotide similarity conflicts with AA similarity. There are many such examples involving other codon families in various mitochondrial genetic codes. Proper codon degeneration will make synonymous codons more similar to each other at the nucleotide level than they are to nonsynonymous codons. Here, I illustrate a “principled” codon degeneration method that achieves these objectives. The method was applied to resolving the mammalian basal lineage and phylogenetic position of rheas among ratites. The codon degeneration method was implemented in the user-friendly and freely available DAMBE software for all known genetic codes (genetic codes 1 to 33).

scholarly journals Neurodegenerative disorders associated with genes of mitochondria

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Vaibhav S. Marde ◽  
Prerna L. Tiwari ◽  
Nitu L. Wankhede ◽  
Brijesh G. Taksande ◽  
Aman B. Upaganlawar ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorders ◽  
Friedreich Ataxia ◽  
Mitochondrial Genes ◽  
Disease Development ◽  
Main Text ◽  
Functional Studies ◽  
Dominant Part ◽  
Causative Link

Abstract Background Over the last decade, aggregating evidences suggested that there is a causative link between mutation in gene associated with mitochondrial dysfunction and development of several neurodegenerative disorders. Main text Recent structural and functional studies associated with mitochondrial genes have shown that mitochondrial abnormalities possibly lead to mitochondrial dysfunction. Several studies on animal models of neurodegenerative diseases and mitochondrial genes have provided compelling evidence that mitochondria is involved in the initiation as well as progression of diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and Friedreich ataxia (FA). Conclusion In this mini-review, we have discussed the different etiologic and pathogenesis connected with the mitochondrial dysfunction and relevant neurodegenerative diseases that underlie the dominant part of mitochondrial genes in the disease development and its progress.

scholarly journals Nuclear Gene Dosage Effects Upon the Expression of Maize Mitochondrial Genes

Genetics ◽  
2001 ◽  
Vol 157 (4) ◽  
pp. 1711-1721
Author(s):  
Donald L Auger ◽  
Kathleen J Newton ◽  
James A Birchler
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Gene Dosage ◽  
Nuclear Gene ◽  
Eukaryotic Cell ◽  
Mitochondrial Genes ◽  
Northern Analysis ◽  
Α Subunit ◽  
Dosage Effects ◽  
A Genome

Abstract Each mitochondrion possesses a genome that encodes some of its own components. The nucleus encodes most of the mitochondrial proteins, including the polymerases and factors that regulate the expression of mitochondrial genes. Little is known about the number or location of these nuclear factors. B-A translocations were used to create dosage series for 14 different chromosome arms in maize plants with normal cytoplasm. The presence of one or more regulatory factors on a chromosome arm was indicated when variation of its dosage resulted in the alteration in the amount of a mitochondrial transcript. We used quantitative Northern analysis to assay the transcript levels of three mitochondrially encoded components of the cytochrome c oxidase complex (cox1, cox2, and cox3). Data for a nuclearly encoded component (cox5b) and for two mitochondrial genes that are unrelated to cytochrome c oxidase, ATP synthase α-subunit and 18S rRNA, were also determined. Two tissues, embryo and endosperm, were compared and most effects were found to be tissue specific. Significantly, the array of dosage effects upon mitochondrial genes was similar to what had been previously found for nuclear genes. These results support the concept that although mitochondrial genes are prokaryotic in origin, their regulation has been extensively integrated into the eukaryotic cell.

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