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Recent discoveries have revealed remarkable complexity within olfactory sensory neurons (OSNs), including the existence of two OSN populations based on the expression of Cd36. However, the regulatory mechanisms governing this cellular diversity in the same cell type remain elusive. Here, we show the preferential expression of 79 olfactory receptors in Cd36 + OSNs and the anterior projection characteristics of Cd36 + OSNs, indicating the non-randomness of Cd36 expression. The integrated analysis of single-cell RNA sequencing (scRNA-seq) and scATAC-seq reveals that the differences in Cd36 +/− OSNs occur at the immature OSN stage, with Mef2a and Hdac9 being important regulators of developmental divergence. We hypothesize that the absence of Hdac9 may affect the activation of Mef2a , leading to the up-regulation of Mef2a target genes, including teashirt zinc finger family member 1 (Tshz1), in the Cd36 + OSN lineage. We validate that Tshz1 directly promotes Cd36 expression through enhancer bindings. Our study unravels the intricate regulatory landscape and principles governing cellular diversity in the olfactory system. [Display omitted] • A subpopulation of olfactory sensory neurons (OSNs) characterized by Cd36 expression • Cd36 + OSNs exhibit unique transcriptome, chromatin, and spatial patterns • Differences in Cd36 + OSNs emerge during the immature OSNs stage with OR selection • Mef2a and Tshz1 contribute to the regulation of cellular difference in Cd36 + OSNs Yang et al. utilized scRNA and scATAC sequencing approaches to characterize the cellular diversity of olfactory sensory neurons (OSNs). The study reveals a distinct OSN subpopulation characterized by CD36 receptor expression, elucidating the regulatory landscape and potential transcription factors that govern these differences. [ABSTRACT FROM AUTHOR]

Lead is a heavy metal pollutant that is widely present in the environment. It affects every organ system, yet the nervous system appears to be the most sensitive and primary target. Although many countries have made significant strides in controlling Pb pollution, Pb poisoning continuous to be a major public health concern. Exposure to Pb causes neurotoxicity that ranges from neurodevelopmental disorders to severe neurodegenerative lesions, leading to impairments in learning, memory, and cognitive function. Studies on the mechanisms of Pb-induced nervous system injury have convincingly shown that this metal can affect a plethora of cellular pathways affecting on cell survival, altering calcium dyshomeostasis, and inducing apoptosis, inflammation, energy metabolism disorders, oxidative stress, autophagy and glial stress. This review summarizes recent knowledge on multiple signaling pathways associated with Pb-induced neurological disorders in vivo and in vitro. • Summarize Pb neural signal transduction in vivo and in vitro. • The pathways are concerned with Pb-induced neurological disorders. • Lead influence on calcium homeostasis can induce multiple neurological disorders. • Lead-induced neurological disorders are characterized by learning and memory disorders. [ABSTRACT FROM AUTHOR]