Sperm aging is accelerated by the buildup of reactive oxygen species (ROS), which cause oxidative damage to various cellular components. Aging can be slowed by limiting the production of mitochondrial ROS and by increasing the production of antioxidants, both of which can be generated in the sperm cell itself or in the surrounding somatic tissues of the male and female reproductive tracts. However, few studies have compared the separate contributions of ROS production and ROS scavenging to sperm aging, or to cellular aging in general. We measured reproductive fitness in two lines of Drosophila melanogaster genetically engineered to (1) produce fewer ROS via expression of alternative oxidase (AOX), an alternative respiratory pathway; or (2) scavenge fewer ROS due to a loss-of-function mutation in the antioxidant gene dj-1β. Wild-type females mated to AOX males had increased fecundity and longer fertility durations, consistent with slower aging in AOX sperm. Contrary to expectations, fitness was not reduced in wild-type females mated to dj-1β males. Fecundity and fertility duration were increased in AOX and decreased in dj-1β females, indicating that female ROS levels may affect aging rates in stored sperm and/or eggs. Finally, we found evidence that accelerated aging in dj-1β sperm may have selected for more frequent mating. Our results help to clarify the relative roles of ROS production and ROS scavenging in the male and female reproductive systems.

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.

We conducted on-site studies in Kyoto City, Japan, to evaluate the effect of air pollution by automobile gas exhaust on the leaf photosynthetic functions of four urban roadside tree species. Nitrogen oxides (NO and NO 2 ) are major air pollutants that are related to automobile gas exhaust. The species-speci c response of leaf photosynthesis to air pollution was obtained for single-year data, in which at the high air pollution sites, Rhododendron × pulchrum, Rhaphiolepis indica, and Prunus × yedoensis had a higher restriction of maximum photosynthesis (A max ), while the opposite trend was obtained for Ginkgo biloba.When the data were pooled across the years from 2007 to 2019 in R. pulchrum, the dose-dependent effect of NO and NO 2 on photosynthesis became obvious, in which they decreased A max and increased the longterm leaf water use e ciency. A spatial variability map for R. pulchrum showed a lower A max and higher water use e ciency at the heavy tra c areas in Kyoto City, which suggests that R. pulchrum increased tolerance to air pollution and water stress at the expense of the leaf photosynthesis. This study revealed the importance of the evaluation of the species-speci c response of photosynthesis to air pollution for the e cient use of urban trees, even in regions with relatively low atmospheric pollution levels such as < 40 ppb of NO or NO 2 .

Animals vary genetically in responses to dietary change. Both mitochondrial and nuclear genomes contribute to this variation, but the role of combinatorial "mito-nuclear" genetic variation is understudied. We do not know whether specific nutrients modify patterns of mito-nuclear variation, nor whether putative epigenetic mechanisms play a role. Here, we show that enriching dietary essential amino acids or lipids modifies patterns of mito-nuclear variation in Drosophila life-history, including transgenerational effects of lipids. Systematically evaluating alternative statistical models revealed that diet-mito-nuclear interactions were a leading driver of phenotypic variation. Mito-nuclear genotype repeatably predicted phenotypic impacts of nutritional changes, but genotypes bearing naturally co-occurring pairs of mitochondria and nuclei did not necessarily outperform novel pairings, suggesting that nutrition-dependent phenotypes cannot easily be optimised by matching mitochondria to coincident nuclear genotypes. These results enhance understanding of how nutrition and genetics sculpt phenotype, with potential implications for human mitochondrial transfer therapies.