A serotonergic axon-cilium synapse drives nuclear signaling to alter chromatin accessibility
Sheu SH, Upadhyayula S, Dupuy V, Pang S, Deng F, Wan J, Walpita D, Pasolli HA, Houser J, Sanchez-Martinez S, Brauchi SE, Banala S, Freeman M, Xu CS, Kirchhausen T, Hess HF, Lavis L, Li Y, Chaumont-Dubel S, Clapham DE. A serotonergic axon-cilium synapse drives nuclear signaling to alter chromatin accessibility. Cell 2022, 185: 3390-3407.e18. PMID: 36055200, PMCID: PMC9789380, DOI: 10.1016/j.cell.2022.07.026.Peer-Reviewed Original ResearchConceptsCA1 pyramidal neuronsChromatin accessibilityPyramidal neuronsSerotonergic axonsEpigenetic statePrimary ciliaHippocampal CA1 pyramidal neuronsChemogenetic stimulationSerotonin receptorsNuclear actinReceptor 6Histone acetylationAxonsChemical synapsesIntercellular communicationRhoA pathwaySynapseNeuronsCiliaSynapsesStimulationPathwayNeurotransmissionReceptorsCOPII with ALG2 and ESCRTs control lysosome-dependent microautophagy of ER exit sites
Liao Y, Pang S, Li W, Shtengel G, Choi H, Schaefer K, Xu C, Lippincott-Schwartz J. COPII with ALG2 and ESCRTs control lysosome-dependent microautophagy of ER exit sites. Developmental Cell 2024, 59: 1410-1424.e4. PMID: 38593803, DOI: 10.1016/j.devcel.2024.03.027.Peer-Reviewed Original ResearchEndoplasmic reticulum exit sitesER exit sitesAmino acid starvationPurified recombinant componentsExit siteProtein sortingSecretory pathwayMammalian cellsNutrient stressCellular conditionsEndoplasmic reticulumGiant unilamellar vesiclesTubular outgrowthsESCRTMicroautophagyNutrient stressorsALG2COPIILysosomesPathwayMTOR inhibitionUnilamellar vesiclesRecombinant componentsFocused ion beam scanning electron microscopyIon beam scanning electron microscopy