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. 2020 Dec 18;6(51):eabd6078. doi: 10.1126/sciadv.abd6078

Fig. 1. Conditional brain-specific Dcaf1 knockout in mice results in perinatal death and defects in brain and lens development.

Fig. 1

(A) Dcaf1 gene deletion and protein depletion in neonatal mouse brains were confirmed by genomic PCR and immunoblotting. (B) Brain-specific Dcaf1 knockout mice died perinatally within 40 hours of birth. Summary of the numbers of embryos and neonates and their proportion (numbers in the brackets) in each age from the mating of Dcaf1f/+;Nestin-Cre and Dcaf1f/f mice. Neonates were sacrificed soon after delivery (<16 hours after birth) for analysis or observed overnight (<40 hours). Four neonates were lost because of cannibalization. (C) H&E staining of the coronal brain sections from control and Dcaf1 knockout P0 mice. VZ, ventricular zone. (D) H&E staining of the horizontal lens sections. (E) IHC staining of the control and Dcaf1 knockout brains at E13.5. Arrowheads indicate the cleaved caspase-3 and TUNEL (terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling)–positive cells. (F) IHC staining of the control and Dcaf1 knockout lens at E14.5.