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Fig. 1 | Molecular Autism

Fig. 1

From: Loss of the Chr16p11.2 ASD candidate gene QPRT leads to aberrant neuronal differentiation in the SH-SY5Y neuronal cell model

Fig. 1

Functional analysis of QPRT in SH-SY5Y cells. a siRNA-mediated knockdown (KD) of QPRT. Cells were transfected with a non-targeting siRNA (siCtrl) and three different siRNAs targeting QPRT (siQ1–siQ3). Transfected cells were differentiated for 11 days followed by morphological analysis. Knockdown of QPRT was confirmed at protein level. Upon QPRT-KD, cells showed a significant decrease of the maximum intersections radius when compared to the non-targeting control, i.e., the maximum complexity of neurites was significantly closer to the cell soma. None of the three KDs differed with respect to the enclosing radius when compared to the non-target control, i.e., the length of the neurites was not different (Additional file 1: Figure S2). Maximum intersections radius: radial distance of the maximum number of intersections from the cell body. Enclosing radius: outer radius intersecting the cell. All p values were corrected for multiple testing using Tukey's HSD correction. b Chemical inhibition of QPRT. Application of the QPRT inhibitor phthalic acid (PA) for 3 days led to a dose-dependent significant increase of cell death in differentiating wild-type SH-SY5Y cells. In proliferating cells, QPRT inhibition did not change the rate of cell death. c Viability assays of CRISPR/Cas9 mediated QPRT-knock out (KO) cells. Percentage of cell death was assessed performing viability assays after 3 days of differentiation showing a significant increase of cell death in both generated QPRT-KO cell lines. d Representative images of QPRT-KO cells after differentiation. KO of QPRT led to observable cell death during 9 days of differentiation but not during proliferation

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