Grant: Project Grant
University of Toronto
$1,017,450.00
Natural and artificial evolution of toxin-receptor interactions
EF 2020-21
Résumé
Large Clostridial toxins (LCTs) are a family of extraordinarily potent bacterial toxins. For example, the most common hospital-acquired diarrhea in developing countries is caused by Clostridioides difficile and its two LCTs TcdA and TcdB. These toxins cause tissue damage by modulating host cell function and behavior in order to promote tissue invasion and proliferation of pathogens. But before doing so, LCTs must gain entry into the cell. They enter human cells by exploiting cell-surface molecules normally present in healthy tissues and use these for docking onto the cell. However, in most cases it is not clear which receptors these toxins use to gain entry. Although recent studies have started to identify receptors for C. difficile toxins, there are many other LCTs whose receptors are not known. In this project, we will use modern genome engineering tools to identify human receptors for multiple LCTs from several different pathogens. We will then characterize at the structural level how LCTs engage their receptors. Finally, we will engineer toxins to bind new receptors on the cell surface in order to develop next-generation therapies for human diseases.
Programme
Project Grant
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
434792
Name
Taipale Mikko
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Microbiology & Infectious Diseases
Projecttitle
Natural and artificial evolution of toxin-receptor interactions
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$1,017,450
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Clostridium Difficile; Crispr/Cas9; Crispr/Cas9 Screening; Large Clostridial Toxins
Abstract
Large Clostridial toxins (LCTs) are a family of extraordinarily potent bacterial toxins. For example, the most common hospital-acquired diarrhea in developing countries is caused by Clostridioides difficile and its two LCTs TcdA and TcdB. These toxins cause tissue damage by modulating host cell function and behavior in order to promote tissue invasion and proliferation of pathogens. But before doing so, LCTs must gain entry into the cell. They enter human cells by exploiting cell-surface molecules normally present in healthy tissues and use these for docking onto the cell. However, in most cases it is not clear which receptors these toxins use to gain entry. Although recent studies have started to identify receptors for C. difficile toxins, there are many other LCTs whose receptors are not known. In this project, we will use modern genome engineering tools to identify human receptors for multiple LCTs from several different pathogens. We will then characterize at the structural level how LCTs engage their receptors. Finally, we will engineer toxins to bind new receptors on the cell surface in order to develop next-generation therapies for human diseases.
Competitiondate
202010
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Taipale, Mikko; Melnyk, Roman
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,017,450~ $0~