ArticleCurrent biology : CB2016
Lamin Mutations Accelerate Aging via Defective Export of Mitochondrial mRNAs through Nuclear Envelope Budding.
Article in Current biology : CB, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 43 citations in OpenAlex.
- Reversing aging-like 3D genome disorganization in abioRxiv : the preprint server for biology · 2026Article
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- Lamin A/C loss promotes R-loop-mediated genomic instability and poor survival in small-cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Age mosaic of gut epithelial cells prevents aging.Nature communications · 2025Article
- Lamin A/C Deficiency Drives Genomic Instability and Poor Survival in Small-Cell Lung Cancer through Increased R-loop Accumulation.bioRxiv : the preprint server for biology · 2025Article
- MAM-STAT3-Driven Mitochondrial CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Loss of nuclear envelope bud formation leads to mitophagy initiation inAutophagy reports · 2025Article
- Review
- Nuclear envelope budding: Getting large macromolecular complexes out of the nucleus.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Article
- Nuclear envelope budding and its cellular functions.Nucleus (Austin, Tex.) · 2023Article
- Centralspindlin proteins Pavarotti and Tumbleweed along with WASH regulate nuclear envelope budding.The Journal of cell biology · 2023Article
- Review
- Somatic nuclear blebbing in Caenorhabditis elegans is not a feature of organismal aging but a potential indicator of germline proliferation in early adulthood.G3 (Bethesda, Md.) · 2023Article
- Nuclear mRNA Export and Aging.International journal of molecular sciences · 2022Review
- Drosophila p38 MAPK interacts with BAG-3/starvin to regulate age-dependent protein homeostasis.Aging cell · 2021Article
- Review
- Disease Modeling with Human Neurons Reveals LMNB1 Dysregulation Underlying DYT1 Dystonia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- Differential Influence of Sample Sex and Neuronal Maturation on mRNA and Protein Transport in Induced Human Neurons.Frontiers in molecular neuroscience · 2020Article
- Organelle aging: Lessons from model organisms.Journal of genetics and genomics = Yi chuan xue bao · 2019Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Defective RNA metabolism and transport are implicated in aging and degeneration [1, 2], but the underlying mechanisms remain poorly understood. A prevalent feature of aging is mitochondrial deterioration [3]. Here, we link a novel mechanism for RNA export through nuclear envelope (NE) budding [4, 5] that requires A-type lamin, an inner nuclear membrane-associated protein, to accelerated aging observed in Drosophila LaminC (LamC) mutations. These LamC mutations were modeled after A-lamin (LMNA) mutations causing progeroid syndromes (PSs) in humans. We identified mitochondrial assembly regulatory factor (Marf), a mitochondrial fusion factor (mitofusin), as well as other transcripts required for mitochondrial integrity and function, in a screen for RNAs that exit the nucleus through NE budding. PS-modeled LamC mutations induced premature aging in adult flight muscles, including decreased levels of specific mitochondrial protein transcripts (RNA) and progressive mitochondrial degradation. PS-modeled LamC mutations also induced the accelerated appearance of other phenotypes associated with aging, including a progressive accumulation of polyubiquitin aggregates [6, 7] and myofibril disorganization [8, 9]. Consistent with these observations, the mutants had progressive jumping and flight defects. Downregulating marf alone induced the above aging defects. Nevertheless, restoring marf was insufficient for rescuing the aging phenotypes in PS-modeled LamC mutations, as other mitochondrial RNAs are affected by inhibition of NE budding. Analysis of NE budding in dominant and recessive PS-modeled LamC mutations suggests a mechanism by which abnormal lamina organization prevents the egress of these RNAs via NE budding. These studies connect defects in RNA export through NE budding to progressive loss of mitochondrial integrity and premature aging.
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