Abstract
The persistence of juvenile-like properties in specific cell types can provide adaptive advantages to stressful environments. In animals, such traits are well described at the organismal level, but their existence and regulation at the cellular level remain poorly understood. Here, using mice with genetically tagged mature olfactory sensory neurons (OSNs), we show that these neurons can retain immature features in response to environmental stress generated by an increased airflow. This delayed maturation is associated with the sustained nuclear expression of the activating transcription factor 5 (ATF5), which we found to be a potential regulator of this neuronal plasticity. In Atf5-deficient mice, this adaptive response fails to occur, leading to the subsequent loss of OSNs under environmental stress. Thus, the identified protective mechanism in the olfactory system may serve to safeguard neuronal integrity and ensure functional adaptation to environmental stress.