Lena Pernas, John C. Boothroyd & colleagues shed new light on the host-pathogen interactions of a globally prevalent and often chronic disease – toxoplasmosis, caused by the parasitic protozoan Toxoplasma gondii. The parasite lives in vacuoles within human cells, and recruits mitochondria to the membranes of the vacuole (the benefit to the parasite is presumed to be a metabolic one). Pernas and colleagues showed that a parasite protein ‘MAF1’ is needed to recruit the mitochondria. MAF1 is only present in two of the toxoplasma strains tested, suggesting that evolutionary niches exist where association with mitochondria is either advantageous or disadvantageous. Also read more in the accompanying synopsis.
Rhodopsin is a photoresponsive protein found in the cells of the retina which is vital for our perception of light. After it is activated by light it must then be degraded or recycled, but some aspects of the recycling pathway are unclear. In new research published this week, Shiuan Wang, Hugo Bellen & colleagues found that in flies, an evolutionarily conserved protein complex called the retromer is required for the recycling of rhodopsins. Interestingly, when retromer subunits were up-regulated, degeneration of photoreceptor cells could be alleviated in some contexts. This could have potential therapeutic uses if it also works in humans.