Sperm mobility denotes the net movement of a sperm population. Previous work implicated mitochondrial function as a basis underlying phenotypic variation in this quantitative trait. Our objective was to determine if mitochondrial function was indeed critical to expression of phenotype. Phenotype was assigned to roosters within a random bred population (n=242). A representative subpopulation (n=40) was used to correlate sperm mobility with oxygen consumption (r=0.83). In contrast, sperm mobility was independent of mitochondrial helix length in a sample of males (n=7) representing the range of phenotype observed within the population. Thus, mitochondrial function rather than number appeared to be critical to expression of phenotype. This hypothesis was tested by ultrastructural analysis of sperm midpieces. Males from the lower and upper tails of the distribution were characterized with high and low proportions of sperm containing aberrant mitochondria in 47 and 4% of the cells respectively. When sperm from average males were allowed to segregate into immobile and mobile subpopulations, 40% of immobile sperm contained aberrant mitochondria. In contrast, only 9% of sperm from the same males contained aberrant mitochondria in non-segregated populations. In conclusion, the mitochoridrion is an organelle that may account for phenotypic differences in sperm mobility. / Graduation date: 2002