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Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity

ABSTRACT: Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity

PROVIDER: PRJNA1222083 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32304815_1.fastq.gz	Fastqsanger.gz
	SRR32304815_2.fastq.gz	Fastqsanger.gz
	SRR32304816_1.fastq.gz	Fastqsanger.gz
	SRR32304816_2.fastq.gz	Fastqsanger.gz
	SRR32304817_1.fastq.gz	Fastqsanger.gz

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Lamin B1 and LAP2β resist cytoskeletal force to maintain lamin A/C meshwork organization and preserve nuclear integrity

Project description:The nuclear lamins are extremely long-lived proteins in most cell types. As a consequence, lamin function cannot be effectively dissected with temporal precision using standard knock-down approaches. Here, we apply the auxin inducible degron (AID) system to rapidly deplete each lamin isoform within one cell cycle and reveal the immediate impacts of lamin loss on the nucleus . Surprisingly, neither acute lamin A/C (LA/C), lamin B1 (LB1), nor lamin B2 (LB2) depletion altered nuclear shape or induced nuclear blebbing, indicating that acute lamin loss is not sufficient to alter nuclear morphology. LB1 depletion is immediately followed by LA/C meshwork disorganization due to actin cytoskeletal forces on the lamina, yet neither LA/C nor LB1 depletion induced nuclear rupturing. We found that the abundant inner nuclear membrane protein LAP2β protects nuclear integrity in the absence of LB1, as depletion of both LB1 and LAP2β induced severe LA/C disorganization and frequent nuclear rupturing. Depolymerization of the actin cytoskeleton halts nuclear rupture in LAP2β- and LB1-depleted nuclei. We conclude that both LB1 and LAP2β resist cytoskeletal force to maintain regular lamin A/C meshwork organization and preserve nuclear integrity.

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Project description:Lamin A/C are nuclear intermediate filament proteins that form a proteinaceous meshwork called lamina beneath the inner nuclear membrane. Mutations in the LMNA gene encoding lamin A/C cause a heterogenous group of inherited degenerative diseases known as laminopathies. Previous studies have revealed altered cell signaling pathways in lamin mutant patient cells, but little is known about the fate of mutant lamin A/C within the cells. Here, we analyzed the turnover of lamin A/C in cells derived from a dilated cardiomyopathy patient with a heterozygous p.S143P mutation in LMNA. We found that transcriptional activation and mRNA levels of LMNA are increased in the primary patient fibroblasts, but that the lamin A/C protein levels remain equal in control and patient cells because of a meticulous interplay between autophagy and the ubiquitin-proteasome system (UPS). Both endogenous and ectopic expression of p.S143P lamin A/C cause significantly reduced activity of UPS and accumulation of K48-ubiquitin chains in the nucleus. Furthermore, K48-ubiquitinated lamin A/C is degraded by compensatory enhanced autophagy, as shown by increased autophagosome formation and binding of lamin A/C to microtubule-associated protein 1A/1B-light chain 3. Finally, a chaperone 4-PBA augmented protein degradation by restoring UPS activity as well as autophagy in the patient cells. In summary, our results suggest that the p.S143P mutant lamin A/C has overloading and deleterious effects on protein degradation machinery and pharmacological interventions with compounds enhancing protein degradation may be beneficial for cell homeostasis.

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