Ring, B. | Search bioRxiv

bioRxiv2026

A National Survey of 205 Canadian Biomedical Research Core Facilities Reveals Structural Challenges and Opportunities for Strengthening Canada's Research Ecosystem

BackgroundCanadian biomedical core facilities (BCFs) provide researchers with access to advanced tools and unique technical expertise, essential for research. However, their role, sustainability, and impact remain poorly understood. We report on the evolution of model and existing state of Canadas 205 BCFs, examining challenges and benefits. MethodsCross referencing of national databases by the Canadian Innovation Fund (CFI), and from data collected by the Canadian Network of Scientific Platforms (CNSP) allowed he identification of BCFs. Hand curation of these lists validated that cores are operational. To ensure cores not listed by CFI/CNSP were captured, research intensive institutions in Canada were independently searched to identify active cores. ResultsThere are currently 205 active and operational BCFs located across 9 provinces, which can be further stratified into 9 technical domains that describe the nature of services they provide. Quebec (80 cores) and Ontario (75 cores) have the highest confluence of BCFs, with Quebec having a higher ratio of cores per capita. ConclusionsWhile our data establishes the ubiquity of Canadian BCFs, we highlight substantial challenges including sustainability, governance, evaluation and the recognition of support for core scientists. Here, we establish a framework to address these challenges and to inform best practice, to optimize creation of impactful, accessible and functional biomedical core facilities.

scientific communication and education↗

bioRxiv2022

Regulation of Klebsiella pneumoniae mucoidy by the bacterial tyrosine kinase Wzc

Klebsiella pneumoniae is a frequent nosocomial pathogen associated with urinary tract infections (UTI), pneumonia, and septicemia. Two lineages of K. pneumoniae have emerged that challenge the treatment of these infections. One lineage includes hypervirulent strains, causing invasive community-acquired infections, and the other encompasses carbapenem-resistant isolates. Non-mucoid, carbapenem-resistant isolates are most frequently isolated from UTI. Therefore, we hypothesized that environmental conditions may drive K. pneumoniae adaptation to the urinary tract. We found that two rmp-positive, hypervirulent strains and two rmp-negative clinical UTI isolates all suppressed mucoidy when cultured in urine compared to rich LB medium without altering capsular polysaccharide (CPS) abundance. We then performed a transposon screen to identify genetic factors through which urine suppresses mucoidy. Due to variations within transposon hits, we performed whole genome sequencing on our hits and found 100% association between secondary mutations in Wzc and increased mucoidy. Wzc is an inner membrane tyrosine kinase that regulates CPS assembly. When Wzc mutations are encoded chromosomally we observed both increased mucoidy and increased cell-free extracellular polysaccharide (EPS). However, when Wzc mutations are expressed in trans we observed increased mucoidy without impacting CPS or cell-free EPS abundance. Functionally, one periplasmic mutation increased Wzc autophosphorylation, while four active site mutations reduced Wzc autophosphorylation. These four active site mutations are also sufficient to increase mucoidy in one of the rmp-negative clinical UTI isolates without affecting EPS abundance. Combined, these data implicate mutation-driven modulation of Wzc activity as a global, rmp-independent mechanism for increasing K. pneumoniae mucoidy, without altering EPS uronic acid content. Wzc activity may represent the lynchpin that coordinates both capsule biosynthesis and mucoidy, explaining why these two phenotypes have been historically intertwined.

microbiology↗