The abstract is read at the publisher; the summary is JClub's.
Deleting SCS7 in Candida albicans depletes hydroxylated sphingolipids and markedly attenuates virulence and caspofungin susceptibility, linking membrane homeostasis to pathogenic fitness.
- Why it matters: Sphingolipid hydroxylation is conserved in fungi and mammals, but divergent enzymes create a selective vulnerability; identifying the fungal regulator could enable targeted antifungals.
- What they did: The authors screened sphingolipid metabolic genes, then used SCS7 ablation to assess membrane organization, cell wall integrity, hyphal morphogenesis, biofilm formation, stress tolerance, and caspofungin response, including in a murine cutaneous infection model.
- The result: In mice, SCS7 deletion reduces fungal burden and hyperinflammation while preserving epidermal barrier integrity; virtual screening identified resveratrol as a Scs7 inhibitor that reproduces defects and synergizes with caspofungin to enhance killing.
The findingWhy it mattersWhat they didThe result
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