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. 2019 May 7;8:e44702. doi: 10.7554/eLife.44702

Figure 5. Transcriptome analysis of optic nerves of Fasn mutant mice reveal oligodendrocyte defects in late stages of maturation, including myelination.

(a, b) GeneOntology analysis depicting biological processes affected by down-regulated (a) and up-regulated (b) transcripts in P14 optic nerves of mutant (cMU) mice. Metacore Pathway analysis showing pathways affected by downregulated (a) and upregulated (b) transcripts in P14 optic nerves of cMU mice. Data points represent the count of regulated transcript for each category and pathway. (c) Heat map of RNA-seq data of CT and cMU optic nerves at P14, depicting Fasn and selected down- and up-regulated modulators of OL differentiation, maturation and myelination (FDR < 0.05). Markers identified by comparison with OLs single cell sequencing data (Marques et al., 2016) are marked with an asterisk. n = 3 mice for cMU, n = 4 mice for CT. CT = control, cMU = conditional mutant, MFOLs = myelin-forming oligodendrocytes, MOLs = mature oligodendrocytes (Marques et al., 2016).

Figure 5—source data 1. Expressed transcripts in optic nerves from control and cMU mice at P14.
DOI: 10.7554/eLife.44702.016

Figure 5.

Figure 5—figure supplement 1. FASN deficiency is correlated with molecular signs of defective oligodendrocyte maturation.

Figure 5—figure supplement 1.

Graph of qRT-PCR analysis of Sox10, Myrf and MBP in optic nerves of P14 CT and cMU mice. Data are normalized to β-actin and to the mean of CTs (unpaired two-tailed two sample Student’s t-test; Sox10: p=0.0385, t = 2.641, n = 4 for CT and n = 4 for cMU; Myrf: p=0.0326, t = 2.765, n = 4 for CT and n = 4 for cMU; MBP: p=0.0078, t = 3.405, n = 6 for CT and n = 5 for cMU), *p<0.05, **p<0.01. Bars represent mean ±SEM. CT = control, cMU = conditional mutant.