Presentation Details
The Endoplasmic Reticulum Protein Canopy1, Plays a Key Role in Vomeronasal Homeostasis and Neuronal Connectivity

Nicholas A.Mathias1, 2, Paolo E.Forni1, 2, 3.

1Biological Sciences, University at Albany, Albany, NY, USA.2The RNA Institute, University at Albany, Albany, NY, USA.3The Center for Neuroscience Research, Albany, NY, USA

Abstract


The molecular identity of neurons is established by differential regulation of unique signaling pathways, which ultimately modulate gene expression/translation. The vomeronasal organ (VNO) comprises two main subtypes of vomeronasal sensory neurons (VSNs), which express either one or two genes from the vomeronasal receptor families V1R or V2R. Recent work on olfactory sensory neurons (OSNs) has suggested that the polymorphism of olfactory receptors (ORs) differentially activates the unfolded protein response (UPR). The UPR is a compensatory mechanism to correct or manage misfolding of proteins in the Endoplasmic Reticulum (ER).  The OSNs utilize the UPR to transform the aminoacidic polymorphisms of the ORs into distinct signatures by changing the expression of cell adhesion and axonal guidance molecules. Through the analysis of single-cell RNA sequencing (scRNA Seq) of wild type VSNs, we found that the V2R-expressing VSNs selectively express the ER protein Canopy1 (Cnpy1) from progenitors throughout maturity. Performing scRNA sequencing on the VSNs of Cnpy1 knockout (KO) mice showed altered UPR activation, together with aberrant transcription of cell adhesion proteins, axonal guidance molecules, and altered expression of ribosomal protein subunits. In line with this, histological observations show changes in connectivity of the VSNs to the accessory olfactory bulb (AOB). Though the vomeronasal organ of Cnpy1 KO mice appears indistinguishable from that of controls in peripubertal mice, by 60 days of age, the V2R expressing neurons display degeneration. Our data suggests that Cnpy1 loss of function has effects on protein synthesis, activation of the UPR, connectivity, and homeostasis of the V2R VSNs.

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