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. 2020 Aug;30(8):1083–1096. doi: 10.1101/gr.265017.120

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© 2020 Nichterwitz et al.; Published by Cold Spring Harbor Laboratory Press

This article, published in Genome Research, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.

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Figure 1. — LCM-seq strategy to reveal cell intrinsic mechanisms of motor neuron vulnerability and resistance in SMA. (A) We used “delta 7” mice (Smn^−/−/SMN2^+/+/SMNΔ7^+/+) as a model for severe SMA and littermates homozygous for murine Smn as controls (Smn^+/+/SMN2^+/+/SMNΔ7^+/+). (B) Pairwise Spearman's correlation on log₁₀-transformed data of all samples per cell type, genotype, and age. (C) Principal component analysis on the whole gene expression data set. (P) Postnatal day; (CNS) central nervous system; (LCM-seq) laser capture microdissection coupled with RNA sequencing; (SC) spinal cord; (CN) cranial nerve; (CN12) hypoglossal nucleus; (CN10) dorsal motor nucleus of the vagus nerve; (CN7) facial nucleus; (CN3/4) oculomotor and trochlear nuclei; (RN) red nucleus; asterisks in A indicate vulnerable cell types in this mouse model; (WGCNA) weighted gene correlation network analysis; (GO) Gene Ontology.