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ER-phagy regulates ER dynamics during myogenesis (5)

ABSTRACT: IP-MS interactome of FAM134B1 and FAM134B2 complexes (bimolecular complementation affinity purification (BiCAP) system)

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Paolo Grumati

LAB HEAD: Paolo Grumati

PROVIDER: PXD050902 | Pride | 2024-12-27

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	2023-07-06_MS_VB_IP_Myoblasts_Fam134b1_V1_V2_1.raw	Raw
	2023-07-06_MS_VB_IP_Myoblasts_Fam134b1_V1_V2_2.raw	Raw
	2023-07-06_MS_VB_IP_Myoblasts_Fam134b1_V1_V2_3.raw	Raw
	2023-07-06_MS_VB_IP_Myoblasts_Fam134b1_V1_V2_4.raw	Raw
	2023-07-06_MS_VB_IP_Myoblasts_Fam134b1_V1_V2_dox_1.raw	Raw

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ER-phagy regulates ER dynamics during myogenesis

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ER-phagy regulates ER dynamics during myogenesis

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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Fam134c and Fam134b shape axonal endoplasmic reticulum architecture in vivo.

Project description:Endoplasmic reticulum (ER) remodeling is vital for cellular organization. ER-phagy, a selective autophagy targeting ER, plays an important role in maintaining ER morphology and function. The FAM134 protein family, including FAM134A, FAM134B, and FAM134C, mediates ER-phagy. While FAM134B mutations are linked to hereditary sensory and autonomic neuropathy in humans, the physiological role of the other FAM134 proteins remains unknown. To address this, we investigated the roles of FAM134 proteins using single and combined knockouts (KOs) in mice. Single KO in young mice showed no major phenotypes, however, combined Fam134b and Fam134c deletion (Fam134b/cdKO), but not the combination including Fam134a deletion, led to rapid neuromuscular and somatosensory degeneration, resulting in premature death. Fam134b/cdKO mice show rapid loss of motor and sensory axons in the peripheral nervous system. Long axons from Fam134b/cdKO mice exhibited expanded tubular ER with a transverse ladder-like appearance, whereas no obvious abnormalities were observed in cortical ER. Our study unveils critical roles of FAM134C and FAM134B in the formation of tubular ER network in axons of both motor and sensory neurons.

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