We cordially invite you to attend the Umeå Infection Symposium on 27 June 2025. Get inspired by the invited keynote speaker and learn about novel research approaches and directions at Umeå University. Registration deadline is Friday 13 June!
There is plenty of time to network at the Umeå Infection Symposium.
ImageMattias Pettersson
Welcome to the symposium!
The symposium is aimed for all scientists and staff members interested in microbial and infection research. The event is jointly organized by The Laboratory for Molecular Infection Medicine Sweden, MIMS, and Umeå Microbial Research Centre, UCMR, at Umeå University.
The scientific symposium takes place on Friday 27 June at 10:00-14:30, including a pre-event coffee from 9:30, and a lunch that gives all participants the opportunity to mingle and continue the scientific discussions. After the end of the symposium, we invite all participants for coffee and cake.
The venue for the symposium is P5 Väven in central Umeå (Storgatan 46 A).
Confirmed keynote speaker
Matthew Chapman is invited keynote speaker from US.
ImageUniversity of Michigan
Matthew Chapman, Ph.D Professor and Associate Chair of Graduate Studies, University of Michigan
Polymerizing the Fiber Between Functional and Pathogenic Amyloid Formation
Amyloids are best known as a hallmark of neurodegenerative diseases like Parkinson’s and Alzheimer’s. However, many organisms can assemble amyloid fibers that are non-toxic and that are intention-built to fulfill functions in the cell. My lab has studied the assembly of such “functional amyloids” and how they might interact with toxic amyloids like those associated with human disease.
Enteric bacteria like E. coli produce curli fibrils, extracellular functional amyloids that are an integral part of the biofilm extracellular matrix. Bacteria tightly regulate the formation of curli fibrils to prevent accumulation of toxic intracellular amyloid intermediates. CsgA is the major proteinaceous component of curli fibrils and contains highly amyloidogenic regions within its five-repeat structure. A chaperone-like protein called CsgC prevents toxic amyloid intermediates from forming in the periplasmic space. At the cell surface during curli formation and in vitro using purified proteins, monomeric CsgA can be recruited into the growing fiber end in seeding process. CsgA is also able to accelerate amyloid-formation by the human protein alpha-synuclein.
To better understand how CsgA impacts alpha-synuclein aggregation, several CsgA homologs were identified and characterized. CsgA homologs from bacteria present in the human microbiome were shown to also accelerate alpha-synuclein aggregation. We also found that CsgC homologs can inhibit CsgA and alpha-synuclein aggregation. CsgC sub-stoichiometrically inhibits CsgA fibrillation and stabilizes an intrinsically disordered form of CsgA in vitro. We show that a highly transient interaction with CsgC is sufficient to delay fibril formation of CsgA. This work will be discussed in the context of bacterial and human protein interactions and their consequences, and also how from the perspective of how the bacteria controls curli amyloid formation to prevent toxicity to its own cellular processes.
10:00-10:15 WELCOME by the Directors Fredrik Almqvist (UCMR) and Oliver Billker (MIMS)
10:15-11:15 KEYNOTE LECTURE
Matthew Chapman, Professor and Associate Chair of Graduate Studies, University of Michigan: Polymerizing the Fiber Between Functional and Pathogenic Amyloid Formation
11:15-11:45 TALK 1
Verena Köhler, new UCMR PI: tba
11:45-12:45 LUNCH
12:45-13:15 TANDEM TALK
Vanja Lundberg Wiraeus, University of Gothenburg, new MIMS Clinical Research Fellow, and Emma Haapaniemi, Group Leader at FIMM, University of Helsinki: tba
13:15-13:45 TALK 2
Chinmay Dwibedi, new UCMR PI, new MIMS Group Leader and DDLS Fellow: tba
13:45-14:15 TALK 3
Tomas N Gustafsson, new UCMR PI and Infectious Disease Physician, Sunderby Hospital: Targeting tularemia and clashing with the claps