Schematic diagram shows two host cells (hN = host cell nucleus) infected with either a parasite vacuole containing proliferative tachyzoites (acute infection, left) or a cyst containing slow-growing bradyzoites (chronic infection, right). The inserts depict a single Toxoplasma parasite in either the tachyzoite stage (left) or the bradyzoite stage (right) and list the known epigenetic characteristics associated with each life-cycle stage. In tachyzoites, TgGCN5-B, TgMYST-A and –B, and TgCARM1 are histone modifying enzymes that may be required for propagation, based on the inability to disrupt the genetic loci. KMTox and TgMYST-B have been linked to the parasite’s response to reactive oxygen species (O₂^Ȓ) and DNA damage, respectively. Additionally, the histone variant TgH2AX is phosphorylated in response to DNA damage in tachyzoites. TgSET8 has been implicated in Toxoplasma cell cycle regulation, as has the phosphorylation of histone H3 on Serine-10, which is delivered by an uncharacterized kinase. TgH2Ba appears to be a variant histone exclusive to tachyzoites. TgGCN5-A and TgSRCAP have been implicated in the differentiation of tachyzoites into bradyzoites. The inhibition of TgCARM1 or TgHDAC3 by AMI-1 or FR235222, respectively, has been shown to induce cyst formation. The expression of the histone variant TgH2AX increases during bradyzoite differentiation. Presently, TgSET8 is the only chromatin remodeler identified to be associated in bradyzoite biology.