Asked by mike
What would happen to a cell if the Golgi apparatus stopped functioning?
All Answers 1
Answered by
GPT-5 mini
AI
Briefly: the cell would rapidly lose its ability to process, sort and send proteins and lipids to their correct destinations. That would cause failures in secretion, membrane maintenance and lysosome function and soon lead to stress and cell death.
Key points
- Loss of secretion and membrane delivery
- Proteins meant for secretion (hormones, enzymes, antibodies, cytokines) would not be packaged into secretory vesicles and would not be delivered to the plasma membrane or extracellular space.
- Delivery of transmembrane proteins (receptors, channels, adhesion molecules) to the cell surface would be impaired, disrupting signaling, transport and cell–cell interactions.
- Failed post-translational modification
- Glycosylation, sulfation and other Golgi modifications would not occur or be incomplete. This changes protein folding, stability, activity and targeting.
- Lysosome biogenesis disrupted
- Lysosomal hydrolases would not be properly tagged and routed to lysosomes, producing dysfunctional lysosomes and accumulation of undegraded substrates (similar to what happens in some lysosomal storage diseases, e.g., I‑cell disease).
- Traffic bottlenecks and ER stress
- Proteins accumulate in the ER and in transport vesicles, provoking ER stress and the unfolded protein response (UPR). Persistent UPR can trigger apoptosis.
- Impaired membrane turnover, polarity and cell division
- Plasma membrane repair and expansion, apical/basal polarity of epithelial cells, and membrane remodeling during cytokinesis would be compromised.
- Cellular and tissue consequences
- Cells highly dependent on secretion (pancreatic acinar cells, plasma cells, neurons, endocrine cells, immune cells) would fail first and tissues/organs would lose function.
- Over time, widespread dysfunction would lead to cell death and tissue pathology.
In short: immediate disruption of secretion and protein/lipid processing, followed by ER stress, organelle dysfunction (notably lysosomes), and often cell death if Golgi function cannot be restored.
Key points
- Loss of secretion and membrane delivery
- Proteins meant for secretion (hormones, enzymes, antibodies, cytokines) would not be packaged into secretory vesicles and would not be delivered to the plasma membrane or extracellular space.
- Delivery of transmembrane proteins (receptors, channels, adhesion molecules) to the cell surface would be impaired, disrupting signaling, transport and cell–cell interactions.
- Failed post-translational modification
- Glycosylation, sulfation and other Golgi modifications would not occur or be incomplete. This changes protein folding, stability, activity and targeting.
- Lysosome biogenesis disrupted
- Lysosomal hydrolases would not be properly tagged and routed to lysosomes, producing dysfunctional lysosomes and accumulation of undegraded substrates (similar to what happens in some lysosomal storage diseases, e.g., I‑cell disease).
- Traffic bottlenecks and ER stress
- Proteins accumulate in the ER and in transport vesicles, provoking ER stress and the unfolded protein response (UPR). Persistent UPR can trigger apoptosis.
- Impaired membrane turnover, polarity and cell division
- Plasma membrane repair and expansion, apical/basal polarity of epithelial cells, and membrane remodeling during cytokinesis would be compromised.
- Cellular and tissue consequences
- Cells highly dependent on secretion (pancreatic acinar cells, plasma cells, neurons, endocrine cells, immune cells) would fail first and tissues/organs would lose function.
- Over time, widespread dysfunction would lead to cell death and tissue pathology.
In short: immediate disruption of secretion and protein/lipid processing, followed by ER stress, organelle dysfunction (notably lysosomes), and often cell death if Golgi function cannot be restored.
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