Systems-Based Analysis of the Sarcocystis neurona Genome Identifies Pathways That Contribute to a Heteroxenous Life Cycle

Blazejewski, Tomasz; Nursimulu, Nirvana; Pszenny, Viviana; Dangoudoubiyam, Sriveny; Namasivayam, Sivaranjani; Chiasson, Melissa A.; Chessman, Kyle; Tonkin, Michelle; Swapna, Lakshmipuram S.; Hung, Stacy S.; Bridgers, Joshua; Ricklefs, Stacy M.; Boulanger, Martin J.; Dubey, Jitender P.; Porcella, Stephen F.; Kissinger, Jessica C.; Howe, Daniel K.; Grigg, Michael E.; Parkinson, John

To survive and persist in their respective hosts, apicomplexan parasites have evolved a variety of molecular strategies. These include a group of specialized proteins that facilitate parasite entry, egress, and colonization, as well as molecular decoys that modulate host immune signaling (4, 5) . The majority of these proteins localize to exocytic organelles (micronemes, rhoptries, and dense granules) that discharge in a highly coordinated program of invasion (5) . For Toxoplasma gondii, initial host recognition and attachment are performed by members of the SAG1-related sequence (SRS) family. This is followed by secretion of the microneme (MIC) proteins that strengthen host cell attachment and result in the formation of a "moving junction" that provides the motive force required to penetrate the host cell. The moving junction is further controlled by a set of proteins known as rhoptry neck (RON) proteins that facilitate invasion (for a review, see reference 6). Subsequently, rhoptry (ROP) proteins and densegranule (GRA) proteins are secreted into the host cytosol to interact with cellular targets to protect the (now) intracellular parasite from clearance. The parasite is further protected through encasement within a parasitophorous vacuole (PV) that is, interestingly, absent from the schizont form of Sarcocystis.