Sac1 links phosphoinositide turnover to cryptococcal virulence

Gaylord, Elizabeth A.; Choy, Hau Lam; Chen, Guohua; Briner, Sydney L.; Doering, Tamara L.

doi:10.1128/mbio.01496-24

Sac1 links phosphoinositide turnover to cryptococcal virulence

Journal Article · Wed Aug 14 00:00:00 EDT 2024 · mBio (Online)

DOI:https://doi.org/10.1128/mbio.01496-24· OSTI ID:2530393

^[1]; ^[2]; Chen, Guohua ^[1]; Briner, Sydney L. ^[1]; ^[1]

Washington University School of Medicine, St. Louis, MO (United States)
Washington University School of Medicine, St. Louis, MO (United States); L.E.K. Consulting, Boston, MA (United States)

Cryptococcus neoformans is an environmentally acquired fungal pathogen that causes over 140,000 deaths per year. Cryptococcal infection occurs when infectious particles are deposited into the lung, where they encounter host phagocytic cells. C. neoformans may be engulfed by these phagocytes, an important step of infection that leads to outcomes ranging from termination of infection to cryptococcal dissemination. To study this critical process, we screened approximately 4,700 cryptococcal gene deletion mutants for altered uptake, using primary mouse and human phagocytic cells. Among the hits of these two screens, we identified 93 mutants with perturbed uptake in both systems, as well as others with differences in uptake by only one cell type. We further screened the hits for changes in thickness of the capsule, a protective polysaccharide layer around the cell which is an important cryptococcal virulence factor. The combination of our three screens yielded 45 mutants, including one lacking the phosphatidylinositol-4-phosphate phosphatase Sac1. In this work, we implicate Sac1 in both host cell uptake and capsule production. We found that sac1 mutants exhibit lipid trafficking defects, reductions in secretory system function, and changes in capsule size and composition. Many of these changes occur specifically in tissue culture media, highlighting the role of Sac1 phosphatase activity in responding to the stress of host-like conditions. Overall, these findings show how genome-scale screening can identify cellular factors that contribute to our understanding of cryptococcal biology and demonstrate the role of Sac1 in determining fungal virulence.

View Accepted Manuscript (DOE)

Research Organization:: University of Georgia, Athens, GA (United States)

Sponsoring Organization:: National Institute of Allergy and Infectious Diseases (NIAID); National Institute of General Medical Sciences (NIGMS); USDOE

Grant/Contract Number:: SC0015662

OSTI ID:: 2530393

Journal Information:: mBio (Online), Journal Name: mBio (Online) Journal Issue: 8 Vol. 15; ISSN 2150-7511

Publisher:: American Society for Microbiology (ASM)Copyright Statement

Country of Publication:: United States

Language:: English

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59 BASIC BIOLOGICAL SCIENCES
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PI4P
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mycology
phosphatase
phosphoinositide
virulence

Sac1 links phosphoinositide turnover to cryptococcal virulence

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