bioRxiv Science⌕ Search

Biology subjects

Sahu, J.

Publications and source records attributed to Sahu, J..

3 recordsLinked to original sources

Mitochondrial genes affect the immune response against bacterial infection (Duck Pasteurellosis) through a cascade of mechanisms mediated by nuclear immune genes- a cross talk with nuclear and mitochondrial gene

Mitochondria possess 37 genes of its own, helpful for carrying out various functions including oxidative phosphorylation. But the mitochondria is neither independent in terms of its structure, nor its function, it depend upon nuclear gene for its functionality and replication. Our lab has earlier reported the role of mitochondrial genome in controlling health and reproduction in animal model. Reports also indicate that mitochondria have role in immune response against bacterial infection. In our current study, we depict the role of two polypeptide coding mitochondrial gene as cytochrome B and cytochrome C in providing host immunity against bacterial disease (Duck Pasteurellosis). We further observe that the mechanism was governed by cascade of mechanisms mediated through nuclear genes NRLP3, IL18 and Sting. In the first phase of the study, we have characterized Cytochrome B and Cytochrome C genes from Bengal duck and quantified through the assesment of the expression profiling with respect to healthy and Pasteurella infected ducks following a natural challenge with Pasteurella multocida. In the next phase of our study, we have characterized the above nuclear genes in Bengal duck and attempted to correlate the expression with mitochondrial genes. We attempted to explore the mechanism of pathway how mitochondrial DNA triggers the nuclear immune response leading to destruction of bacterial pathogen. Molecular docking revealed how IL18 directly binds with the pathogen. This is the first report in animal model.

genomics↗

Role of NUMTs (Nuclear mitochondrial DNA) genes in affecting disease resistance in duck against Pasteurellosis

Ducks are mostly resistant to common avian diseases, but frequent occurrence of duck pasteurellosis, commonly kown as Duck Cholera, caused by Pasteurella multocida may cause a loss. In our earlier studies, we have identified certain immune response genes of nuclear origin as well as mitochondrial genes in duck, conferring resistance against duck cholera. In our current study, we have detected certain NUMT (Nuclear mitochondrial) genes in duck with certain role in disease resistance in case of duck cholera. NUMT genes are basically nuclear genes, but they act through mitochondria. Identified NUMT genes (Thymidine phosphorylase/ endothelial cell growth factor1 gene, TFAM Transcription factor A, mitochondrial, TK2 Thymidine kinase 2) were characterized and certain important domains were identified. Differential mRNA expression profiling revealed upregulation of the genes in healthy ducks compared to that of infected ducks. Exploitation of the identified genes may lead to development of ducks resistant to duck Cholera.

genomics↗

Adaptations of energy metabolism in cetaceans have consequences for their response to foraging disruption

Cetaceans have varied their anatomical structure, physiology and metabolism to adapt to the challenges of aquatic life. Key to this change is the deposition of blubber. This adipose tissue plays a significant regulatory and signaling role in mammalian metabolism. As foraging disruption by human activities is emerging as a key conservation threat for cetaceans, we need to understand how selection for aquatic life might have altered key nutrient sensing pathways associated with adipose signaling. We compared selection pressure on those energy metabolism biological pathways by contrasting the rate of substitution observed in genes associated with them in cetacean and artiodactyl genomes. We then estimated the likely consequence of these selection pressures for pathway functions. Here we show that genes involved in the insulin, mTOR, SIRT and NF-{kappa}B pathways were under significant positive selection in cetaceans compared to their terrestrial sister taxon. Our results suggest these genes may have been positively selected to adapt to a glucose-poor diet and it is unlikely that fat depots signaling function in the same manner as in terrestrial mammals. Secondary adaptation to life in water significantly affected functions in nutrient sensing pathways in cetaceans. Insulin is not likely to play the same role in energy balance as it does in terrestrial mammals and adiposity is not likely to have the deleterious health consequences it has in terrestrial mammals. The physiological ecology of cetacean fat deposition, and therefore its value as a condition index, needs to be interpreted in this evolutionary context.

evolutionary biology↗