Scientists discover molecular shredder in deadly parasite

Researchers at the University of York have identified a protein called ESB2 that acts as a molecular shredder, enabling the African trypanosome parasite to evade the human immune system. The parasite, which causes sleeping sickness, uses ESB2 to precisely edit its genetic instructions in real time. This breakthrough solves a 40-year mystery in the parasite's biology.

The African trypanosome covers itself with a protective layer of variant surface glycoproteins, or VSG, to survive in the human bloodstream. However, it produces far more of these cloak proteins than the helper proteins encoded alongside them. Dr. Joana Faria, head of the research group at the University of York, explained that ESB2, located in the parasite's Expression Site Body, cuts apart instructions for helper genes while sparing those for the VSG cloak, as genetic instructions are processed there. The study, published in Nature Microbiology, reveals this mechanism allows the parasite to remain undetected by the host's immune system. Lianne Lansink, first author, said: 'When we first saw the molecular shredder localised in the microscope, we knew we had found something special.' Dr. Faria called it a full-circle moment, noting the puzzle had lingered since her postdoc days. The work, funded by a Sir Henry Dale Fellowship from the Wellcome Trust and Royal Society, involved researchers from the UK, Portugal, the Netherlands, Germany, Singapore, and Brazil. Sleeping sickness, transmitted by tsetse flies, can lead to confusion, disrupted sleep, and coma without treatment, affecting sub-Saharan Africa.

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Realistic illustration of spinning hemozoin crystals inside a malaria parasite propelled by hydrogen peroxide reactions, like tiny rockets.
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Scientists identify a rocket-fuel-like reaction that propels spinning iron crystals inside malaria parasites

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University of Utah researchers report that iron-rich hemozoin crystals inside the malaria parasite Plasmodium falciparum move through the parasite’s digestive compartment because reactions involving hydrogen peroxide at the crystal surface generate chemical propulsion. The work, published in Proceedings of the National Academy of Sciences, links a long-observed phenomenon to peroxide chemistry and could point to new antimalarial drug strategies and ideas for engineered micro- and nanoscale devices.

Researchers have discovered a protein called Aurora-related kinase 1 (ARK1) that is vital for the malaria parasite's cell division. Disabling ARK1 in experiments halted the parasite's ability to replicate in both human and mosquito hosts. The finding, published in Nature Communications, highlights a potential target for new antimalarial drugs.

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Researchers at Caltech have discovered how viruses infect bacteria by disabling a key protein called MurJ, essential for cell wall construction. This mechanism, revealed through high-resolution imaging, suggests a new approach to combating antibiotic-resistant superbugs. The findings highlight convergent evolution in unrelated viruses blocking MurJ similarly.

Researchers at Cold Spring Harbor Laboratory have found that blocking the protein PTP1B improves memory and boosts plaque clearance in mouse models of Alzheimer's disease. The discovery links the protein to brain immune function and metabolic risks like diabetes and obesity. The team aims to develop inhibitors for potential human treatments.

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Researchers at UCLA Health and UC San Francisco have identified a natural defense mechanism in brain cells that helps remove toxic tau protein, potentially explaining why some neurons resist Alzheimer's damage better than others. The study, published in Cell, used CRISPR screening on lab-grown human neurons to uncover this system. Findings suggest new therapeutic avenues for neurodegenerative diseases.

Researchers at the University of California San Diego report they have developed a second-generation CRISPR-based “Pro-Active Genetics” system, called pPro-MobV, that is designed to spread between bacteria and disable antibiotic-resistance genes, including inside hard-to-treat biofilms.

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