A5091330898- Genetics, Aging, and Longevity in Model Organisms
- Endoplasmic Reticulum Stress and Disease
- Autophagy in Disease and Therapy
- Mitochondrial Function and Pathology
- Tryptophan and brain disorders
- Fungal and yeast genetics research
- Circadian rhythm and melatonin
- Genetic Neurodegenerative Diseases
- Prion Diseases and Protein Misfolding
- Aging, Elder Care, and Social Issues
- Photosynthetic Processes and Mechanisms
- Adipose Tissue and Metabolism
- Nanoparticles: synthesis and applications
Rutgers, The State University of New Jersey
2017-2024
Rutgers Sexual and Reproductive Health and Rights
2020-2023
Rütgers (Germany)
2020-2023
neurons under stress can produce giant vesicles, several microns in diameter, called exophers. Current models suggest that exophers are neuroprotective, providing a mechanism for stressed to eject toxic protein aggregates and organelles. However, little is known of the fate exopher once it leaves neuron. We found produced by mechanosensory
In human neurodegenerative diseases, neurons can transfer toxic protein aggregates to surrounding cells, promoting pathology via poorly understood mechanisms.
Abstract Toxic protein aggregates can spread among neurons to promote human neurodegenerative disease pathology. We found that in C. elegans touch intermediate filament proteins IFD-1 and IFD-2 associate with aggresome-like organelles are required cell-autonomously for efficient production of neuronal exophers, giant vesicles carry away from the neuron origin. The we identified juxtanuclear, HttPolyQ aggregate-enriched, dependent upon orthologs mammalian aggresome adaptor proteins, dynein...
Toxicity of misfolded proteins and mitochondrial dysfunction are pivotal factors that promote age-associated functional neuronal decline neurodegenerative disease across species. Although these neurotoxic challenges have long been considered to be cell-intrinsic, considerable evidence now supports human originating in one neuron can appear neighboring cells, a phenomenon proposed pathology spread disease. C. elegans adult neurons express aggregating extrude large (~4 µm) membrane-surrounded...
ABSTRACT While autophagy is key to maintain cellular homeostasis, tissue-specific roles of individual genes are less understood. To study neuronal in vivo , we inhibited specifically C. elegans neurons, and unexpectedly found that knockdown early-acting genes, i.e., involved formation the autophagosome, except for atg-16.2 decreased PolyQ aggregates increased lifespan, albeit independently degradation autophagosomal cargo. Neuronal can be secreted from neurons via vesicles called exophers,...
Toxicity of misfolded proteins and mitochondrial dysfunction are pivotal factors that promote age-associated functional neuronal decline neurodegenerative disease across species. Although these neurotoxic challenges have long been considered to be cell-intrinsic, considerable evidence now supports human originating in one neuron can appear neighboring cells, a phenomenon proposed pathology spread disease. C. elegans adult neurons express aggregating extrude large (~4 µm) membrane-surrounded...
Abstract Under conditions of proteostasis disequilibrium, neurons can enhance intracellular and extracellular protective mechanisms to guard against neurotoxicity. In mammals, an response severe imbalance that results from proteosome inhibition is the formation juxtanuclear intermediate filament-surrounded, aggregate-filled aggresomes, which sequester threatening aggregates for later disposal via lysosomal degradation. Highly proteo-stressed also engage assistance neighboring cells in...
ABSTRACT C. elegans neurons under stress can produce giant vesicles, several microns in diameter, called exophers. Current models suggest that exophers are neuroprotective, providing a mechanism for stressed to eject toxic protein aggregates and organelles. However, little is known of the fate exopher once it leaves neuron. We found produced by mechanosensory engulfed surrounding hypodermal skin cells then broken up into numerous smaller vesicles acquire phagosome maturation markers, with...