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• W4310361220 abstract "Summary Gasdermin D (GSDMD) and mixed lineage kinase domain-like protein (MLKL) are the pore-forming effectors of pyroptosis and necroptosis, respectively, with the capacity to disturb plasma membrane selective permeability and induce programmed cell death. The budding yeast Saccharomyces cerevisiae has long been used as a simple eukaryotic model for the study of proteins associated with human diseases by heterologous expression. In this work, we expressed in yeast both GSDMD and its N-terminal domain [GSDMD(NT)] to characterize their cellular effects, and compare them to those of MLKL. GSDMD(NT) and MLKL inhibited yeast growth, formed cytoplasmic aggregates, and fragmented mitochondria. Loss-of-function point mutants of GSDMD(NT) showed affinity for this organelle. Besides, GSDMD(NT) and MLKL caused an irreversible cell cycle arrest through TORC1 inhibition, and disrupted endosomal and autophagic vesicular traffic. Our results provide a basis for a humanized yeast platform to study GSDMD and MLKL, a useful tool for structure-function assays and drug discovery." @default.
• W4310361220 created "2022-12-09" @default.
• W4310361220 creator A5029415610 @default.
• W4310361220 creator A5065602595 @default.
• W4310361220 creator A5073054776 @default.
• W4310361220 date "2022-11-29" @default.
• W4310361220 modified "2023-10-16" @default.
• W4310361220 title "Human Gasdermin D and MLKL disrupt mitochondria, endocytic traffic and TORC1 signaling in budding yeast" @default.
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• W4310361220 doi "https://doi.org/10.1101/2022.11.29.518328" @default.
• W4310361220 hasPublicationYear "2022" @default.
• W4310361220 type Work @default.

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