A critical role for glycine betaine in the schizogonic proliferation of the protozoan parasite Perkinsus olseni

Abstract Protozoan parasites in the genus Perkinsus proliferate within marine mollusc hosts through schizogony to produce intracellular daughter cells. This proliferation of P. olseni PRA-181 requires glycine betaine (GB) derived from host molluscs. Although GB exhibits diverse biochemical functions, its role in promoting cell proliferation is unique, and its underlying mechanism is unclear. In the GB-supplemented medium, trophozoite enlargement and DNA replication were completed by Day 3, followed by the initiation of daughter cell budding after Day 4 and their release by Day 8. In contrast, GB-free medium supported cell enlargement and DNA replication but failed to induce daughter cell formation. GB exerted its strongest effect at 68 h after inoculation, corresponding to the onset of daughter cell formation. Trophozoites pre-cultured for 12 days in a GB-free medium initiated proliferative division within 48 h of exposure to GB-supplemented seawater. The timing of GB responsiveness suggested that GB affected the late G1 or S phase. These findings indicated that the host-derived GB was associated with a specific regulatory point controlling daughter cell formation downstream of DNA replication (i.e. karyokinesis or cytokinesis) in P. olseni PRA-181, providing novel insights into the host–parasite interaction and parasitism strategy of this species.