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The complete mitochondrial (mt) genome of the Korean field mouse Apodemus peninsulae was sequenced and found to be 16,266 bp in length. The mt protein-coding genes of A. peninsulae had ATG, GTG, ATC, and ATA as initiation codons and TAA, TAG, TA, and T as termination codons. Two forms each of trnL and trnS and the three tRNA clusters, IQM, WANCY, and HSL were identified, as in the typical Rodentia mt genome. Among tRNAs, abnormal cloverleaf structure of trnS((AGY)) was identified in DHU arm. The l-strand replication origin has the potential to form a stable stem-loop structure and control region has several conserved sequence elements.

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Mitochondria, the energy-producing organelles of the eukaryotic cell, originate from an endosymbiotic  -proteobacterium. Genome architecture and gene content of mitochondrial DNA (mtDNA) vary extensively throughout eukaryotes. New insights into early mitochondrial genome evolution come from the investigation of primitive mitochondriate eukaryotes, as well as from the comparison between mitochondria and intracellular bacterial symbionts. In this work, the size of circular mitochondrial (mt) genome from the marine sponge Suberites domuncula (Porifera, Demospongiae), representative of the oldest and most simple metazoan phylum, was defined to be ~25 kilobases (kb). Primary structure of 2 portions of mtDNA (>14 kb in total ; >55% of the mt genome) was analysed and the DNA sequences of 8 complete and 2 incomplete protein genes, 12 genes for transfer RNAs and a 3' portion od 16S ribosomal RNA gene were determined. In its compact organisation and well-conserved animal-like gene order this poriferan mtDNA resembles those of the other Metazoa. However, mt genome in sponge S. domuncula contains the gene for subunit 9 of the F0-ATP synthase (located in the nucleus in all other multicellular animals) and encodes bacterial-like ribosomal and transfer RNAs. The genetic code in S. domuncula mt genes is minimally derived and only the UGA termination codon is used to code for triptophan.

The plant mitochondrial genome (mtDNA) has long presented a puzzle to plant molecular biologists. The research has fallen far behind that of the other organelle DNAs. An important event that increased the interest in the study of the plant mtDNA was the finding that the genetic determinants responsible for the cytoplasmic male sterile (cms) phenotype were located in the mitochondrial genome (Leaver and Gray, 1982; Levings, 1983; Laughnan and Gabay-Laughnan, 1983; Sederoff, 1984). Cms was shown in many cases to segregate along with mtDNA modifications as observed on restriction enzyme profile. This stimulated an extensive effort to study the plant mitochondrial genome. As a result, we have now begun to understand its organization. The early literature reporting the use of restriction enzymes revealed a very complex organization for the plant mitochondrial genome (Quetier and Vedel, 1977). Those complex mtDNA restriction enzyme profiles with submolar and multimolar bands, which led to the idea of genomic molecular heterogeneity has reinvigorated interest in studying plant mtDNA structure by electron microscopy. Unfortunately, a broad size range of mostly linear molecules was visualized, probably representing artefacts of the isolation procedure as it was not possible as yet to isolate intact mtDNA molecules. Closed circular mtDNA molecules represented only a few percent of the total and were of diverse size (Quetier and Vedel, 1977; Levings and Pring, 1978; Levings et al., 1979). For maize, the circles could be graphed into discrete size classes of different abundance (Levings et al., 1979). It is only through the approach of cloning technology during the last six years that the structure of the plant mt genome has been elucidated. It is indeed a complex organization where recombination between repeated sequences plays an important role.

The nuclear mmg1 mutation, which reduces rho − mutability in Saccharomyces cerevisiae , renders the rho + cells less sensitive to inactivation by nitrous acid (NA) but has little or no effect on the NA sensitivity of the rho 0 cells devoid of mitochondrial (mt) DNA. Therefore the cells' NA sensitivity seems to be influenced by an interaction of the mmg1 mutation and the mt genome rather than the mmg1 mutation itself. The clonal variation of NA sensitivity is high in MMG + yeast and significantly reduced in rho 0 mutants and mmg1 cells. The results presented suggest that frequent spontaneous heritable changes of the mt genome occur in MMG + cells, which, (i) unlike rho − mutations, do not damage the respiratory capacity, and (ii) manifest themselves in a high clonal variation of NA sensitivity.

Objective: To understand role of mitochondrial (mt) mutations in genes regulating oxidative phosphorylation (OXPHOS) in pathogenesis of male infertility. Infertility affects approximately 15% of couples trying to conceive. Infertility is frequently attributed to defects of sperm motility and number. Mitochondrion and mitochondrial DNA (mtDNA) play an important role in variety of physiological process. They control the oxidative energy supply and thus are central to growth, development and differentiation. Mitochondrial function is controlled by a fine-tuned crosstalk between mtDNA and nuclear DNA (nDNA). As mitochondria supply energy by OXPHOS, any mutation in mtDNA disrupts adenosine triphosphate (ATP) production and thus result in an impaired spermatogenesis and impaired flagellar movement. As sperm midpiece has few mtDNA copies, thus enhanced number of mutant mtDNA results in early phenotypic defect which manifest as spermatogenic arrest or asthenozoospermia. Oxidative stress and mtDNA mutations are positively correlated and mutations in mitochondrial genome (mt genome) are implicated in the lowered fertilising capacity of the sperm and affects the reproductive potential of an individual. Materials and Methods: A thorough review of articles in the last 15 years was cited with reference to the below-mentioned keywords. The articles considered discuss the role of mt genome in the normal functioning of sperm and the factors associated with mt mutations and impact of these mutations on the reproductive potential. Results: Sperm motility is a very important factor for the fertilisation of ova. The energy requirements of sperm are therefore very critical for sperm. Mutations in the mitochondrial genes as COX II, ATPase 6 and 8 play an important role and disrupts ATP production affecting the spermatogenesis and sperm motility. Therefore, the aberrations in mt genome are an important etiopatholgy of male infertility. Conclusion: In the context of male infertility, mt mutations, generation of reactive oxygen species and lowered antioxidant capacity are interlinked and constitute a unified pathogenic molecular mechanism. In the era of assisted reproduction technique (ART), it is very important to distinguish between mutations in nuclear and mitochondrial genomes in sperm, as mtDNA mutations are better diagnostic and prognostic markers in infertile men opting for ART.