RT Journal Article
SR Electronic
T1 Toxoplasma ERK7 defends the apical complex from premature degradation
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2021.12.09.471932
DO 10.1101/2021.12.09.471932
A1 William J. O’Shaughnessy
A1 Xiaoyu Hu
A1 Sarah Ana Henriquez
A1 Michael L. Reese
YR 2023
UL http://biorxiv.org/content/early/2023/02/06/2021.12.09.471932.abstract
AB Accurate cellular replication balances the biogenesis and turnover of complex structures. In the apicomplexan parasite Toxoplasma gondii, daughter cells form within an intact mother cell, creating additional challenges to ensuring fidelity of division. The apical complex is critical to parasite infectivity and consists of apical secretory organelles and specialized cytoskeletal structures. We previously identified the kinase ERK7 as required for maturation of the apical complex in Toxoplasma. Here we define the Toxoplasma ERK7 interactome, including a putative E3 ligase, CSAR1. Genetic disruption of CSAR1 fully suppresses loss of the apical complex upon ERK7 knockdown. Furthermore, we show that CSAR1 is normally responsible for turnover of maternal cytoskeleton during cytokinesis, and that its aberrant function is driven by mislocalization from the parasite residual body to the apical complex. These data identify a protein homeostasis pathway critical for Toxoplasma replication and fitness and suggest an unappreciated role for the parasite residual body in compartmentalizing processes that threaten the fidelity of parasite development.Competing Interest StatementThe authors have declared no competing interest.