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. 2001 Feb 1;21(3):788–797. doi: 10.1523/JNEUROSCI.21-03-00788.2001

Fig. 9.

Fig. 9.

Postnatal loss of Dnmt1-deficient brain cells in mutant mice with maternal inheritance of the nestin-cre transgene.A, Southern blot analysis of the Dnmt1gene deletion in DNA from different brain regions of mutant mice after maternal inheritance of the nestin-cre transgene. At the newborn stage ∼30–35% of Dnmt1 gene deletion was detected in both mutant and heterozygous brains. FB, Forebrain;Col, colliculus; CB, cerebellum;BS, brainstem; SP, spinal cord.B, Dnmt1-deficient brain cells are eliminated during postnatal development. Deletion of the Dnmt1 gene was maximal by E12.5 (Br, whole brain) and remained constant in the brain throughout the late stage of embryogenesis and at the postnatal day 1 (P1; also see A). However, only a very small number of cells (4–6%) carrying theDnmt1 deletion was detected in the cortex (CX) and cerebellum (CB) in 2-week-old (P14) mutant mice. By P21, Dnmt1-deficient cells were not detectable by Southern blot analysis in the cortex, cerebellum, or other regions of the brain (data not shown).mutant, Mutant mice with theNestin-cre;Dnmt12lox/N genotype.con, Control samples fromNestin-cre;Dnmt1+/2lox mice, which showed constant levels of the Dnmt1 deletion at P1 and P21.