Abstract
Reproduction is essential to perpetuate life. Animals must utilize strategies in order to allocate the necessary resources for the energy-costly process of reproducing. Here, we show that C. elegans with mutation in alh-6, a conserved mitochondrial proline catabolism gene known to cause mitochondrial defects show a diet-independent decline in fertility. These animals have altered expression of metabolism and male-reproduction genes and display several sperm-specific defects. We identify that PRDH-1 is essential to confer these phenotypes and identify key metabolites and molecules that influence this premature reproductive senescence. Altogether, our data reveal new insights in reproductive aging and describes how important proper mitochondrial function is for reproductive capacity.