التفاصيل البيبلوغرافية
| العنوان: |
Non-cell autonomous regulation of cell-cell signaling and differentiation by mitochondrial ROS. |
| المؤلفون: |
Yipeng Du1, Lei Wang1, Perez-Castro, Lizbeth2, Conacci-Sorrell, Maralice2, Sieber, Matthew1 matthew.sieber@utsouthwestern.edu |
| المصدر: |
Journal of Cell Biology. 12/2/2024, Vol. 223 Issue 12, p1-S7. 30p. |
| مصطلحات موضوعية: |
*CELL receptors, *MITOCHONDRIA, *NOTCH genes, *REACTIVE oxygen species, *CELL membranes, *GENETIC transcription |
| مستخلص: |
Mitochondrial reactive oxygen species (ROS) function intrinsically within cells to induce cell damage, regulate transcription, and cause genome instability. However, we know little about how mitochondrial ROS production non-cell autonomously impacts cell-cell signaling. Here, we show that mitochondrial dysfunction inhibits the plasma membrane localization of cell surface receptors that drive cell-cell communication during oogenesis. Within minutes, we found that mitochondrial ROS impairs exocyst membrane binding and leads to defective endosomal recycling. This endosomal defect impairs the trafficking of receptors, such as the Notch ligand Delta, during oogenesis. Remarkably, we found that overexpressing RAB11 restores ligand trafficking and rescues the developmental defects caused by ROS production. ROS production from adjacent cells acutely initiates a transcriptional response associated with growth and migration by suppressing Notch signaling and inducing extra cellualr matrix (ECM) remodeling. Our work reveals a conserved rapid response to ROS production that links mitochondrial dysfunction to the non-cell autonomous regulation of cell-cell signaling. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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