Toxoplasma gondii is a microscopic parasite that infects all mammals, including humans. The parasite normally inhabits felines but can be transferred to humans from contact with cat feces and eating undercooked meat and unwashed vegetables. Current estimates indicate that 30% of the United States is infected with the parasite. First time infection of Toxoplasma in pregnant women is the leading cause of birth defects in the United States, and infection of people with weak immune systems, such as AIDS and transplant patients, often results in death. Toxoplasma is also related to the parasite that causes malaria, therefore knowing how the parasite grows may allow for the development of new drugs that can treat not only toxoplasmosis, but malaria as well. When the COPS7B gene activity, which is involved in controlling protein degradation, is increased in human cells infected with T. gondii, Toxoplasma grows much slower in host cells than it does in cells with normal COPS7B gene levels. We hypothesize that the parasite uses degraded components of host proteins to make its own proteins and when COPS7B levels are high, degradation is impeded. We hope to evaluate this hypothesis by precisely comparing the growth and invasion efficiency of parasites in modified and normal cells, as well as the corresponding protein degradation status