Abstract
Certain insects (e.g., moths and butterflies; order Lepidoptera) and nematodes are considered as excellent experimental models to study the cellular stress signaling mechanisms since these organisms are far more stress-resistant as compared to mammalian system. Multiple factors have been implicated in this unusual response, including the oxidative stress response mechanisms. Radiation or chemical-induced mitochondrial oxidative stress occurs through damage caused to the components of electron transport chain (ETC) leading to leakage of electrons and generation of superoxide radicals. This may be countered through quick replacement of damaged mitochondrial proteins by upregulated expression. Since the ETC comprises of various proteins coded by mitochondrial DNA, variation in the composition, expressivity and regulation of mitochondrial genome could greatly influence mitochondrial role under oxidative stress conditions. Therefore, we carried out in silico analysis of mitochondrial DNA in these organisms and compared it with that of the stress-sensitive humans/mammals. Parameters such as mitochondrial genome organization, codon bias, gene expressivity and GC(3) content were studied. Gene arrangement and Shine-Dalgarno (SD) sequence patterns indicating translational regulation were distinct in insect and nematodes as compared to humans. A higher codon bias (ENC≫35) and lower GC(3) content (≫0.20) were observed in mitochondrial genes of insect and nematodes as compared to humans (ENC>42; GC3>0.20), coupled with low codon adaptation index among insects. These features indeed favour higher expressivity of mitochondrial proteins and might help maintain the mitochondrial physiology under stress conditions. Therefore, our study indicates that mitochondrial genome organization may influence stress-resistance of insects and nematodes.
Highlights
A number of physical/chemical stress agents increase the cellular ROS/RNS pool and subsequently cause significant biomolecular damage
Since mitochondria are a major source of cellular ROS/RNS, successful maintenance of a healthy cellular redox state through mitochondrial tolerance is considered an important determinant of cellular fate under such conditions
Stress-induced increase in mitochondrial ROS/RNS generation occurs mainly through damage caused to the components of electron transport chain (ETC), thereby resulting in leakage of electrons and the subsequent formation of superoxide radical
Summary
A number of physical/chemical stress agents increase the cellular ROS/RNS pool and subsequently cause significant biomolecular damage. Stress-induced increase in mitochondrial ROS/RNS generation occurs mainly through damage caused to the components of electron transport chain (ETC), thereby resulting in leakage of electrons and the subsequent formation of superoxide radical. This damage may be countered through increase in expression and replacement of the damaged proteins by the newly synthesized functional molecules. Since the mitochondrial genome codes for a number of proteins participating in oxidative phosphorylation and all tRNAs, it is pertinent to expect that evolutionary variations known to occur in the organization and functioning/ regulation of mitochondrial genome amongst different organisms [1, 2, 3, 4] may cause variation in the mitochondrial functions including their role in cellular stress response
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