Cell Nonautonomous Proteostasis
Cell Nonautonomous Proteostasis - Related Videos
10:36
In Vivo Imaging of Transgenic Gene Expression in Individual Retinal Progenitors in Chimeric Zebrafish Embryos to Study Cell Nonautonomous Influences
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Cited by 2 •
2017
Live tracking of individual WT retinal progenitors in distinct genetic backgrounds allows for the assessment of the contribution of cell non-autonomous signaling during neurogenesis. Here, a combination of gene knockdown, chimera generation via embryo transplantation and in vivo time-lapse confocal imaging was utilized for this purpose.
08:59
4D Imaging of Protein Aggregation in Live Cells
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Cited by 4 •
2013
Cellular viability depends on timely and efficient management of protein misfolding. Here we describe a method for visualizing the different potential fates of a misfolded protein: refolding, degradation, or sequestration in inclusions. We demonstrate the use of a folding sensor, Ubc9ts, for monitoring proteostasis and aggregation quality control in live cells using 4D microscopy.
03:03
Fluorescent Reporter-Based Paralysis Assay: A Technique to Assess Age-Associated Progressive Formation of Polyglutamine Fluorescent Reporter and Associated Paralysis in Caenorhabditis elegans
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2025
This video demonstrates an in vivo imaging-based assay to determine proteostasis decline due to aging. The assay uses Caenorhabditis elegans expressing polyglutamine YFP-fusion protein in body wall muscles to measure the age-associated aggregation of polyglutamine and induction of proteotoxicity, leading to paralysis.
10:04
Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
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2025
This protocol describes the in vivo reprogramming of mouse cancer cells into type 1 dendritic-like cells within the tumor microenvironment through enforced expression of the transcription factors PU.1, IRF8, and BATF3.
22:06
Derivation of Hematopoietic Stem Cells from Murine Embryonic Stem Cells
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Cited by 8 •
2007
This protocol details the derivation of transplantable hematopoietic stem cells from mouse embryonic stem cells (ESC) and their subsequent injection into lethally irradiated recipient mice. Briefly, ESC are differentiated as embryoid bodies, which are then infected with retroviral HoxB4 and co-cultured with OP9 stromal cells and hematopoietic cytokines.
FAQs
Neuronal, endocrine, and secreted-factor pathways can carry information from a stressed tissue to distant cells. Their importance lies in converting a local proteotoxic event into a coordinated response rather than leaving each tissue to react independently. This signaling architecture helps explain how stress responses can extend across tissues in an organism.
Distant cells may respond by activating molecular chaperones, the unfolded protein response, or autophagy. These responses address protein-folding and protein-clearance challenges through distinct cellular programs, although the supplied context does not specify how one is selected over another. Measuring which response is activated can therefore reveal how tissues react to incoming stress signals.
Cell nonautonomous proteostasis matters because the effect of proteotoxic stress is not necessarily confined to the tissue where misfolded or damaged proteins arise. Signaling to other tissues can strengthen organism-wide resistance, making intercellular coordination a central biological feature rather than a secondary consequence of local protein quality control.
Biological studies can follow how a stress in one tissue is linked to responses in another, then identify whether neuronal, endocrine, or secreted-factor signaling is involved. The key outcome is a map of communication between tissues and the associated activation of chaperones, the unfolded protein response, or autophagy.
Aging, infection, and metabolic stress provide distinct contexts for asking whether tissues coordinate protein-quality responses. Research in these settings can assess how organism-wide resistance changes when proteotoxic pressure affects one or more tissues. This makes the topic relevant to biology beyond analyses focused only on a single cell or tissue.
In neurodegenerative disease research, the framework directs attention beyond protein handling within affected cells. Investigators can ask whether signals from other tissues activate protective programs, including chaperones, the unfolded protein response, or autophagy, and whether that coordination contributes to cellular resilience. It therefore connects disease biology with organism-level stress regulation.