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Updated: Aug 16, 2025
Multi-Photon Laser Ablation of Cytoplasmic Microtubule Organizing Centers in Mouse Oocytes
Published on: November 11, 2022
Dissection of the autophagic route in oocytes from atretic follicles
Abraham Castro-Cruz1, Olga M Echeverría1, Luis Sánchez-Sánchez2
1Laboratorio de Microscopía Electrónica, Departamento de Biología Celular, Facultad de Ciencias, Universidad Nacional Autónoma de México,Ciudad Universitaria, Col. Universidad Nacional Autónoma de México, Coyoacán, Ciudad de México, México.
Background Information:
Autophagy is a conserved process that functions as a cytoprotective mechanism; it may function as a cell death process called programmed cell death type II. There is considerable evidence for the presence of autophagic cell death during oocyte elimination in prepubertal rats. However, the mechanisms involved in this process have not been deciphered.
Results:
Our observations revealed autophagic cell death in oocytes with increased labeling of the autophagic proteins Beclin 1, light chain 3 A (LC3 A), and lysosomal-associated membrane protein 1 (Lamp1). Furthermore, mTOR and phosphorylated (p)-mTOR (S2448) proteins were significantly decreased in oocytes with increased levels of autophagic proteins, indicating autophagic activation. Moreover, phosphorylated protein kinase B (p-AKT) was not expressed by oocytes, but mitogen-activated protein kinase/extracellular signalregulated kinase (MAPK/ERK) signaling was observed. Additionally, selective and elevated mitochondrial degradation was identified in altered oocytes.
Conclusions:
All these results suggest that mTOR downregulation, which promotes autophagy, could be mediated by low energy levels and sustained starvation involving the phosphoinositide 3-kinase (PI3K)/AKT/mTOR and MAPK/ERK pathways.
Significance:
In this work, we analyzed the manner in which autophagy is carried out in oocytes undergoing autophagic cell death by studying the behavior of proteins involved in different steps of the autophagic pathway.
Insights
Autophagy mediates oocyte elimination in rats via programmed cell death type II. This study deciphers the mechanisms, revealing mTOR downregulation and MAPK/ERK signaling in autophagic cell death.
Area of Science:
- Cell Biology
- Developmental Biology
- Reproductive Biology
Background:
- Autophagy is a conserved cytoprotective process, potentially acting as programmed cell death type II.
- Autophagic cell death is implicated in oocyte elimination in prepubertal rats, but mechanisms remain unclear.
Purpose of the Study:
- To investigate the molecular mechanisms of autophagic cell death during oocyte elimination.
- To analyze the role of key proteins and signaling pathways in this process.
Main Methods:
- Observation of autophagic cell death in oocytes.
- Analysis of autophagic proteins (Beclin 1, LC3 A, Lamp1).
- Assessment of mTOR, p-mTOR, p-AKT, and MAPK/ERK signaling pathways.
- Identification of mitochondrial degradation.
Main Results:
- Increased levels of Beclin 1, LC3 A, and Lamp1 indicate autophagic cell death.
- Decreased mTOR and p-mTOR suggest autophagic activation.
- MAPK/ERK signaling was observed, while p-AKT was absent.
- Selective mitochondrial degradation was evident in altered oocytes.
Conclusions:
- mTOR downregulation, promoting autophagy, may be mediated by low energy and starvation.
- The PI3K/AKT/mTOR and MAPK/ERK pathways are likely involved in regulating autophagy during oocyte elimination.
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