Autophagy-Mediated Degradation of Integumentary Tapetum Is Critical for Embryo Pattern Formation
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ABSTRACT:
PROVIDER: PRJNA1045268 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26949314_1.fastq.gz | Fastqsanger.gz | |||
| SRR26949314_2.fastq.gz | Fastqsanger.gz | |||
| SRR26949315_1.fastq.gz | Fastqsanger.gz | |||
| SRR26949315_2.fastq.gz | Fastqsanger.gz | |||
| SRR26949316_1.fastq.gz | Fastqsanger.gz |
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Project description:Autophagy is a catabolic membrane trafficking process involved in degradation of cellular constituents through lysosomes, which maintains cell and tissue homeostasis. While much attention has been focused on autophagic turnover of cytoplasmic materials, little is known regarding the role of autophagy in degrading nuclear components. Here we report that autophagy machinery mediates degradation of nuclear lamina in mammalian cells, a process we term laminophagy. The autophagy protein LC3 is present in the nucleus and directly interacts with the nuclear lamina protein Lamin B1, and associates with lamin-associated domains (LADs) on chromatin. This interaction does not downregulate Lamin B1 during starvation, but mediates nuclear lamina degradation upon tumorigenic insults, such as by oncogenic Ras. Laminophagy is achieved by nucleus-to-cytosol transport that delivers Lamin B1 to lysosome for degradation. Inhibiting autophagy or LC3-Lamin B1 interaction prevents oncogenic Ras-induced Lamin B1 loss and delays oncogene-induced cell cycle arrest. Our study unveils a role of autophagy in degrading nuclear materials, and suggests laminophagy as a guarding mechanism protecting cells from tumorigenesis.
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