Led by postdoc Frank Bürmann, Jan Löwe’s group in the LMB’s Structural Studies Division, and Mark Dillingham’s group at the University of Bristol, have identified the mechanism the bacterial SMC complex MukBEF uses to entrap DNA ahead of loop extrusion, and found how this pathway can be inhibited by a bacteriophage protein.
Insight on Research
Writing the LINE-1s: How does LINE-1 remodel human DNA to insert its sequence throughout the genome?
Spearheaded by postdoc George Ghanim, Kelly Nguyen’s group in the LMB’s Structural Studies Division have investigated the molecular mechanisms which allow LINE-1 to propagate throughout the genome via retrotransposition during target-primed reverse transcription.
Asgard archaea proteins reveal evolutionary secrets of membrane remodelling
Studying Asgard archaea, Buzz Baum’s group in the LMB’s Cell Biology Division and Aurelien Roux’s group at the University of Geneva, provide insights into the earliest origins of ESCRT-III and reveal how its proteins work together to remodel membranes.
Newly identified quality control mechanism of RNA Polymerase II transcription
Ana Tufegdžić Vidaković’s group, in the LMB’s PNAC Division, have worked with Scott Berry’s group, at the University of New South Wales, to identify the mechanism cells use to regulate gene expression via control of quality and quantity of Pol II molecules.
Discovery of a factor that accelerates protein deliveries to the endoplasmic reticulum
Huping Wang and Manu Hegde, in the LMB’s Cell Biology Division, have found a factor that helps nascent secretory and membrane proteins quickly access the protein translocation machinery when they arrive at the endoplasmic reticulum.
Cryo-ET reveals new molecular insights into tau pathology in Alzheimer’s disease
Benjamin Ryskeldi-Falcon’s group in the LMB’s Neurobiology Division have used cryo-ET to discover that tau filaments are tethered to the membranes of extracellular vesicles in Alzheimer’s disease. These findings introduce membrane tethering of amyloid filaments as a potential target to interfere with their accumulation in disease.