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Comparaison of left and right cervical motoneurons transcriptome

ABSTRACT: Left and Right phrenic nerves, which innervate the left and right diaphragm muscles, exhibit different innervation patterns. This left/right (L/R) asymmetry is established at the onset of innervation by a developmental program that requires Nodal. Phenotype analysis suggests that the cervical motoneurons, which innervate the diaphragm, have a L/R imprint that contributes to set the L/R asymmetries of innervation. We used microarray to analyze the expression profile of left and right cervical motoneurons before diaphragm innervation

ORGANISM(S): Mus musculus

PROVIDER: GSE84778 | GEO | 2017/06/08

SECONDARY ACCESSION(S): PRJNA331128

REPOSITORIES: GEO

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Mus musculus

Project description:Comparaison of left and right cervical motoneurons transcriptome

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Left-right asymmetry of maturation rates in human embryonic neural development

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Intermediolateral column, medial, and lateral motoneurons

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Project description:Although neuronal subtypes often display unique synaptic organization and function, the underlying transcriptional differences necessary to establish these features is poorly understood. To identify molecular pathways that establish synaptic diversity, single neuron PatchSeq RNA profiling was performed on Drosophila tonic and phasic glutamatergic motoneurons. Tonic motoneurons form weaker facilitating synapses onto single muscles, while phasic motoneurons form stronger depressing synapses onto multiple muscles. Super-resolution microscopy and in vivo imaging demonstrated synaptic active zones in phasic motoneurons are more compact and display enhanced Ca2+ influx compared to their tonic counterparts. Genetic analysis identified unique synaptic properties that mapped onto gene expression differences in several cellular pathways, including distinct signaling ligands, post-translational modifications and intracellular Ca2+ buffers. These findings provide insights into how unique transcriptomes can drive functional and morphological differences between two closely related neuronal subgroups.

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Project description:Spinocerebellar ataxia type 7 (SCA7) is an autosomal dominant neurological disorder caused by a deleterious CAG repeat expansion in the coding region of the ataxin-7 gene. The number of CAG repeats determines the severity and age of onset of the disease. Infantile onset SCA7 leads to severe clinical manifestations including dysphagia, aspiration pneumonia and respiratory distress, but the exact cause of respiratory impairment remains unclear. Using the infantile SCA7 mouse model – the SCA7266Q/5Q mouse, we examined the impact of mutant ataxin-7 on the respiratory control centers. Specifically, we examined the effect of pathological poly-Q-ataxin-7 expression on hypoglossal (XII) and phrenic motor units. Further, we identified the transcript profile of the medulla and cervical spinal cord and, investigated the XII and phrenic nerve structure as well as the neuromuscular junctions in the diaphragm and tongue. SCA-7 astrocytes showed significant intranuclear and cytoplasmic inclusions of ataxin-7 in the XII and putative phrenic motor nuclei. Transcriptomic analysis revealed dysregulation of genes involved in amino acid and neurotransmitter transportation, and myelination. Additionally, SCA7 mice demonstrated blunted efferent output of the XII nerve and demyelination in both XII and phrenic nerves. Finally, there was an increased number of NMJ clusters with higher expression of synaptic markers in SCA7 mice compared to WT controls. Thus, pathological ataxin-7 expression disrupts myelination and neurotransmitter transportation, and impairs glial cell function in the respiratory control centers. These pre-clinical findings elucidate the underlying pathophysiology responsible for dysphagia, aspiration and respiratory failure in infantile SCA7.

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