We welcome you to join us in Edinburgh for a chance to network with colleagues and share your cutting-edge Cryptosporidium research.

DEADLINE FOR ABSTRACT SUBMISSION: NOVEMBER 7th Event Timing: December 8th 9am-5pm December 9th 9am-12pm Event Address: The Francis Crick Institute Questions? please email ada...

Cryptosporidium is an important threat to public health, yet it lacks a robust genetic toolkit. Here, Watson et al. introduce a targeted CRISPR-based screening method to identify parasite genes that a...

The epithelial layer that lines the digestive system serves as the primary barrier to infection by intestinal pathogens. While this layer has evolved complex molecular mechanisms to identify and respo...

FIKK effector kinases underwent rapid evolutionary expansion and are a druggable target in Plasmodium falciparum.

Researchers at the Francis Crick Institute have shown that the Cryptosporidium parasite exports a protein into infected intestinal cells, altering the gut environment and enabling the parasite to surv...

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.