Meiotic chromosomal defects increase with age and are a major cause of miscarriages and age-related fertility loss in women. The link between maternal age and fertility has been well studied, however it is unknown if, and, how germline integrity impacts the rate of aging of the whole organism. We are utilizing the nematode model Caenorhabditis elegans to address the causative role of germline health on somatic aging. Specifically, we have examined genes that govern meiotic fidelity in the germline and addressed their role in somatic aging. C. elegans is uniquely suited to address this question as the somatic cells in the adult organism are post mitotic, allowing us to selectively disrupt germline integrity through meiotic gene mutations. We found that 14 of the 38 mutations we examined, in genes that govern different steps of meiosis, significantly reduced the lifespan of the animal. We also found that germline-specific RNAi knockdown of selected meiotic gene candidates,
spo-11,
dsb-2, and
htp-3, also reduced lifespan. These genes have roles throughout meiosis including double strand break formation during the process of meiotic recombination (
spo-11 and
dsb-2) and the formation of the synaptonemal complex (
htp-3). We also examined how meiotic gene disruption impacts the rate of aging by measuring healthpsan parameters. We found mutations in all of the selected candidate meiotic genes, exhibited deficits in at least one, and often more than one, healthspan feature, including loss of mobility, diminished pharyngeal muscle pumping, tissue integrity and neurological function. Overall, our data demonstrate that genes that govern meiotic fidelity in the C. elegans germline impact the physiological health of the somatic tissues and aging of the whole organism.