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Bettinazzi, S.

Publications and source records attributed to Bettinazzi, S..

3 recordsLinked to original sources

Mitochondrial metabolism and body condition of naturally infected sunfish (Lepomis gibbosus)

Parasites can affect host behavior, cognition, locomotion, body condition and many other physiological traits. Changes to host aerobic metabolism are likely responsible for these parasite-induced performance alterations. Whole-organism metabolic rate is underpinned by cellular energy metabolism driven most prominently by the mitochondria. However, few studies have explored how mitochondrial enzymatic activity relates to body condition and parasite infection despite being a putative site for metabolic disruptions related to health status. We studied correlations among natural parasite infection, host body condition and the activity of key mitochondrial enzymes in target organs from wild-caught pumpkinseed sunfish (Lepomis gibbosus) to better understand the cellular responses of fish hosts to endoparasite infection. Enzymatic activities in the gills, spleen, and brain of infected fish were not significantly related to parasite infection or host body condition. However, the activity of cytochrome C oxidase, an enzyme involved in oxidative phosphorylation, in fish hearts was higher in individuals with lower body condition. Activities of citrate synthase, complexes I and III and carnitine palmitoyltransferase were also significantly different among organ types. These results provide preliminary information regarding the likely mitochondrial pathways affecting host body condition, the maintenance energetic requirements of different organs and their specific dependency on particular mitochondrial pathways. These results help pave the way for future studies on the effects of parasite infection on mitochondrial metabolism.

ecology↗

Evolutionary trajectories are contingent on mitonuclear interactions

Critical mitochondrial functions, including cellular respiration, rely on frequently interacting components expressed from both the mitochondrial and nuclear genomes. The fitness of eukaryotic organisms depends on a tight collaboration between both genomes. In the face of an elevated rate of evolution in the mitochondrial genome, current models predict that maintenance of mitonuclear compatibility relies on compensatory evolution of the nuclear genome. Mitonuclear interactions would therefore exert an influence on evolutionary trajectories. One prediction from this model is that the same nuclear genomes but evolving with different mitochondrial haplotypes would follow distinct molecular paths towards higher fitness peaks. To test this prediction, we submitted 1344 populations derived from seven mitonuclear genotypes of Saccharomyces cerevisiae to more than 300 generations of experimental evolution in conditions that either select for a mitochondrial function, or that do not strictly require respiration for survival. Performing high-throughput phenotyping and whole-genome sequencing on independently evolved individuals isolated from endpoint populations, we identified numerous examples of gene-level evolutionary convergence among populations with the same mitonuclear background. Phenotypic and genotypic data on strains derived from this evolution experiment identify the nuclear genome and the environment as the main determinants of evolutionary divergence, but also show a modulating role for the mitochondrial genome exerted both directly and via interactions with the two other components. We finally recapitulated a subset of prominent loss-of-function alleles in the ancestral backgrounds and confirmed a generalized pattern of mitonuclear-specific and highly epistatic fitness effects. Together, these results demonstrate how mitonuclear interactions can dictate evolutionary divergence of populations with identical starting nuclear genotypes.

evolutionary biology↗

MTALTND4, a second protein coded by nd4 impacts mitochondrial bioenergetics

Recent evidence suggests that the coding potential of the mitogenome is underestimated. We found a downstream alternative ATG initiation codon in the +3 reading frame of the human mitochondrial nd4 gene. This newly characterized alternative open reading frame (altORF) encodes a 99-amino acids long polypeptide, MTALTND4, which is conserved in primates. This small protein is localized in mitochondria and cytoplasm and is also found in the plasma, and it impacts mitochondrial physiology. Alternative mitochondrial peptides such as MTALTND4 may offer a new framework for the investigation of mitochondrial functions and diseases.

molecular biology↗