We are looking for a talented and enthusiastic Postdoctoral researcher to join the Young lab to investigate secreted proteins during chronic Toxoplasma gondii infection.

imageimageDespite their clinical relevance, bradyzoite-filled cysts - the hallmark of chronic toxoplasmosis - are largely overlooked in current diagnostics. This study highlights bradyzoite serologica...

Here the authors demonstrate that the assembly of mitochondrial respiratory supercomplex (III2–IV) from Toxoplasma gondii is critical for parasite fitness. They reveal the basis for cytochrome b inhib...

To survive and multiply in different host niches, malaria parasites require sets of proteins that are expressed during the life cycle in a timely manner. Plasmodium malariae is a human malaria parasit...

Cryptosporidium is an apicomplexan parasite that causes diarrhoeal disease. The species C. parvum is zoonotic and causes significant morbidity and mortality for both humans and farm animals; most comm...

Blood-stage Plasmodium falciparum parasites rely on a non-photosynthetic plastid, the apicoplast, for survival, making it an attractive target for antimalarial intervention. Like the mitochondrion, th...

Cryptosporidium is a common intestinal infection of vertebrates and a significant threat to public health. Within the epithelial layer of the intestine, the parasite invades and replicates. Infected cells are readily detected under the microscope by the presence of elongated microvilli, particularly around the vacuole where the parasite resides. Here, we identify a family of Cryptosporidium virulence factors that are exported into the host cell during infection and localise to the microvilli. We examine the trafficking and function of the most highly expressed family member, MVP1, which appears to control the elongation of microvilli through engagement of host EBP50 and CDC42. Remarkably, this mechanism closely mirrors that of an enteropathogenic Escherichia coli virulence factor, MAP, which is also known to drive host microvilli elongation during infection. This highlights a unique instance where eukaryotic and prokaryotic virulence factors have convergently evolved to modulate host actin structures through a similar mechanism. ### Competing Interest Statement The authors have declared no competing interest.

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