William J. Sullivan

This study shows that H2A.X in Toxoplasma gondii is not essential for DNA damage response but regulates cell cycle progression and virulence gene expression.

This paper shows that GCN5a loss in Toxoplasma gondii promotes latency by causing telomere dysfunction and altering gene expression during differentiation.

This study shows that RAD51 is essential for Toxoplasma gondii tachyzoite replication and that its inhibition leads to replication stress and bradyzoite differentiation.

This study identifies cap-independent translation as a mechanism driving stress-induced differentiation in Toxoplasma gondii by regulating BFD1 protein synthesis.