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Somatic production of reactive oxygen species does not predict its production in sperm cells across Drosophila melanogaster lines

OBJECTIVE: Sperm ageing has major evolutionary implications but has received comparatively little attention. Ageing in sperm and other cells is driven largely by oxidative damage from reactive oxygen species (ROS) generated by the mitochondria. Rates of organismal ageing differ across species and ar...

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Detalles Bibliográficos
Autores principales: Turnell, Biz R., Kumpitsch, Luisa, Ribou, Anne-Cécile, Reinhardt, Klaus
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8028716/
https://www.ncbi.nlm.nih.gov/pubmed/33827685
http://dx.doi.org/10.1186/s13104-021-05550-7
Descripción
Sumario:OBJECTIVE: Sperm ageing has major evolutionary implications but has received comparatively little attention. Ageing in sperm and other cells is driven largely by oxidative damage from reactive oxygen species (ROS) generated by the mitochondria. Rates of organismal ageing differ across species and are theorized to be linked to somatic ROS levels. However, it is unknown whether sperm ageing rates are correlated with organismal ageing rates. Here, we investigate this question by comparing sperm ROS production in four lines of Drosophila melanogaster that have previously been shown to differ in somatic mitochondrial ROS production, including two commonly used wild-type lines and two lines with genetic modifications standardly used in ageing research. RESULTS: Somatic ROS production was previously shown to be lower in wild-type Oregon-R than in wild-type Dahomey flies; decreased by the expression of alternative oxidase (AOX), a protein that shortens the electron transport chain; and increased by a loss-of-function mutation in dj-1β, a gene involved in ROS scavenging. Contrary to predictions, we found no differences among these four lines in the rate of sperm ROS production. We discuss the implications of our results, the limitations of our study, and possible directions for future research. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-021-05550-7.