1. PTEN deletion in mouse facial motoneurons induces somatic, axonal, and nerve hypertrophy, synaptic terminal enlargement, and reduced whisker movement.
2. PTEN deletion positively regulates facial nerve regeneration and recovery of whisker movement after injury.
3. In adult mice, PTEN deletion induces hair loss and facial hyperplasia of the epidermis, suggesting detrimental consequences when reaching adulthood.
The article is generally reliable and trustworthy as it provides a comprehensive overview of the effects of PTEN deletion in mouse facial motoneurons on neuronal morphology, physiology, pathology, and axon regeneration after injury. The authors provide evidence for their claims through experiments conducted on both male and female mice with or without peripheral facial nerve injury. Furthermore, they discuss potential risks associated with PTEN ablation such as tumor formation in the skin or facial hyperplasia in adult mice.
However, there are some points that could be improved upon to make the article more reliable. For example, the authors do not explore any counterarguments to their claims or present any evidence for potential alternative explanations for their findings. Additionally, they do not discuss any possible limitations of their study or provide any information about potential sources of bias that could have affected their results. Finally, while the authors mention that PTEN inhibition is a key driver of successful CNS axon regeneration after optic nerve or spinal cord injury, they do not provide any evidence to support this claim or discuss how this relates to their findings regarding PNS axon regeneration after PTEN deletion from facial motoneurons.