"Gasping for Air: Why Oxygen Deprivation Disrupts the Rough Endoplasmic Reticulum"

"Gasping for Air: Why Oxygen Deprivation Disrupts the Rough Endoplasmic Reticulum"

Why does rough endoplasmic disrupt when oxygen is removed from the cell?

Endoplasmic Reticulum (ER):

The endoplasmic reticulum (ER) is an organelle within eukaryotic cells that plays an essential role in protein synthesis and processing. The rough endoplasmic reticulum (RER) is named for its ribosome-studded surface, which allows it to synthesize and process membrane and secreted proteins. In this article, we will explore why the rough endoplasmic reticulum disrupts when oxygen is removed from the cell.

Protein Synthesis:

The process of protein synthesis in the RER requires oxygen, which is used to generate ATP through cellular respiration. The ATP is then used as a source of energy for the protein synthesis machinery in the RER. When oxygen is removed from the cell, the cells are no longer able to generate ATP, and the protein synthesis machinery in the RER comes to a halt.

However, the ribosomes on the surface of the RER continue to produce proteins despite the lack of ATP. This can lead to an accumulation of partially synthesized proteins in the RER, which can disrupt the normal structure of the organelle.

Furthermore, the accumulation of partially synthesized proteins in the RER can lead to the activation of the unfolded protein response (UPR) pathway. The UPR is a cellular stress response that is activated when there is an accumulation of misfolded or unfolded proteins in the ER. This response aims to restore ER homeostasis by reducing the load of unfolded proteins and increasing the capacity of the ER to process and fold proteins.

However, if the UPR response is prolonged, it can cause ER stress and lead to cell death. This is because the UPR response can activate cell death pathways when it becomes overwhelmed and cannot restore ER homeostasis.

In conclusion, the rough endoplasmic reticulum disrupts when oxygen is removed from the cell because protein synthesis machinery in the RER requires ATP generated through cellular respiration. The accumulation of partially synthesized proteins in the RER can disrupt the normal structure of the organelle and activate the UPR pathway. While the UPR pathway is a critical stress response, prolonged activation can lead to ER stress and cell death. Understanding the effects of oxygen deprivation on the RER can help us better understand the importance of cellular respiration and protein synthesis for cellular function and survival.


#Endoplasmic Reticulum
#Rough Endoplasmic Reticulum
#Oxygen deprivation
#ATP
#Protein synthesis
#Cellular respiration
#Unfolded protein response
#ER stress
#Cell death
#Cellular function.