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ER-phagy regulates ER dynamics during myogenesis

ABSTRACT: Proteomic landscape of human myoblasts and differentiated myotubes

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Paolo Grumati

LAB HEAD: Paolo Grumati

PROVIDER: PXD050898 | Pride | 2024-12-27

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	2022-03-18_MS_DIA_PG_hMyoblastsT0_1.raw	Raw
	2022-03-18_MS_DIA_PG_hMyoblastsT0_2.raw	Raw
	2022-03-18_MS_DIA_PG_hMyoblastsT0_3.raw	Raw
	2022-03-18_MS_DIA_PG_hMyoblastsT10_1.raw	Raw
	2022-03-18_MS_DIA_PG_hMyoblastsT10_2.raw	Raw

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Project description:Endoplasmic reticulum (ER) plasticity and ER-phagy are intertwined processes essential for maintaining ER dynamics. We investigated the interplay between two isoforms of the ER-phagy receptor FAM134B in regulating ER remodeling in differentiating myoblasts. During myogenesis, the canonical FAM134B1 is degraded, while its isoform FAM134B2 is transcriptionally upregulated. The switch, favoring FAM134B2, indicates its significance as a regulator of ER morphology during myogenesis. FAM134B2 partial reticulon homology domain, with its rigid conformational characteristics, enables an efficient ER reshaping. FAM134B2 action increases in the active phase of differentiation leading to ER restructuring via ER-phagy, which then reverts to physiological levels when myotubes are mature and the ER reorganized. Knocking out both FAM134B isoforms in myotubes results in aberrant proteome landscape and the formation of dilated ER structures, both of which are rescued by FAM134B2 re-expression. Our results underscore how the fine tuning of FAM134B isoforms and ER-phagy orchestrate the ER dynamics during myogenesis providing insights into the molecular mechanisms governing ER homeostasis in muscle cells.

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