Fig. 4 | Nature Communications

Fig. 4

From: In vivo epigenetic editing of Sema6a promoter reverses transcallosal dysconnectivity caused by C11orf46/Arl14ep risk gene

Fig. 4The alt text for this image may have been generated using AI.

Selection of targeted genes by C11orf46-SETDB1 complex. a Mouse neuroblastoma cells NSC34 inducibly expressing C11orf46 shRNA upon doxycycline addition (schematic in left panel); selected subset of 17 differentially expressed genes implicated in axonal growth and development was tested in RNA expressed from NSC34:Tet-On C11orf46 shRNA cell (right panel). b Neuronal progenitors received control or C11orf46 shRNA and GFP marker plasmids at somatosensory cortex by IUE at E15; four days later at P0 GFP-positive cells were collected by fluorescence-activated cell sorting (FACS). c C11orf46 transcript levels were reduced by 50% in sorted GFP-positive cortical neurons electroporated with C11orf46 shRNA1 as compared to GFP-positive neurons with control shRNA (P = 0.0003). Note increase of Sema6a transcript upon C11orf46 knockdown (P = 0.0085). *P < 0.05, **P < 0.01, ***P < 0.001 determined by Student’s t-test test. n = 10–19 independent mice per condition. All data were normalized by the Hprt transcript. Bar graphs indicate mean ± S.E.M (a, c)

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