Relaxed selection on male mitochondrial genes in DUI bivalves eases the need for mitonuclear coevolution

Abstract Background Four ohnologous genes (sox1, sox2, sox3, and sox15) were generated by two rounds of whole-genome duplication in a vertebrate ancestor. In eutherian mammals, Sox1, Sox2, and Sox3 participate in central nervous system (CNS) development. Sox15 has a function in skeletal muscle regeneration and has little functional overlap with the other three ohnologs. In contrast, the frog Xenopus laevis and zebrafish orthologs of sox15 as well as sox1-3 function in CNS development. We previously reported that Sox15 is involved in mouse placental development as neofunctionalization, but is pseudogenized in the marsupial opossum. These findings suggest that sox15 might have evolved with divergent gene fates during vertebrate evolution. However, knowledge concerning sox15 in other vertebrate lineages than therian mammals, anuran amphibians, and teleost fish is scarce. Our purpose in this study was to clarify the fate and molecular evolution of sox15 during vertebrate evolution. Results We searched for sox15 orthologs in all vertebrate classes from agnathans to mammals by significant sequence similarity and synteny analyses using vertebrate genome databases. Interestingly, sox15 was independently pseudogenized at least twice during diversification of the marsupial mammals. Moreover, we observed independent gene loss of sox15 at least twice during reptile evolution in squamates and crocodile-bird diversification. Codon-based phylogenetic tree and selective analyses revealed an increased dN/dS ratio for sox15 compared to the other three ohnologs during jawed vertebrate evolution. Conclusions The findings revealed an asymmetric evolution of sox15 among the four ohnologs during vertebrate evolution, which was supported by the increased dN/dS values in cartilaginous fishes, anuran amphibians, and amniotes. The increased dN/dS value of sox15 may have been caused mainly by relaxed selection. Notably, independent pseudogenizations and losses of sox15 were observed during marsupial and reptile evolution, respectively. Both might have been caused by strong relaxed selection. The drastic gene fates of sox15, including neofunctionalization and pseudogenizations/losses during amniote diversification, might be caused by a release from evolutionary constraints.

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Neurodegenerative disorders associated with genes of mitochondria

Future Journal of Pharmaceutical Sciences ◽

10.1186/s43094-021-00215-5 ◽

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.

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Publisher Correction: Relaxed selection underlies genome erosion in socially parasitic ant species

Nature Communications ◽

10.1038/s41467-021-23950-y ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Lukas Schrader ◽

Hailin Pan ◽

Martin Bollazzi ◽

Morten Schiøtt ◽

Fredrick J. Larabee ◽

...

Keyword(s):

Relaxed Selection

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Nuclear Gene Dosage Effects Upon the Expression of Maize Mitochondrial Genes

Genetics ◽

10.1093/genetics/157.4.1711 ◽

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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