Skip to main content
. 2019 Mar 12;6(1):ENEURO.0356-18.2019. doi: 10.1523/ENEURO.0356-18.2019

Figure 2.

Figure 2.

Two standard Cre drivers display differential recombination of the Ldb1 locus in the dorsal telencephalon. A–C, Expression of Ldb1 mRNA and the Ai9 reporter in E12.5 control (A), Emx1Cre;Ldb1lox/lox;Ai9 (B), and NesCre;Ldb1lox/lox;Ai9 (C) brains. A’–C’, Cartoons indicating the domain of Cre activity in the respective conditions. In each condition, Ai9 fluorescence faithfully reports Cre activity in the expected domains. However, Ldb1 expression is seen in a medio-lateral gradient in the dorsal telencephalon of Emx1Cre;Ldb1lox/lox;Ai9 embryos (B) and persists in the entire dorsal telencephalon in NesCre;Ldb1lox/lox;Ai9 brains (C). In contrast, the ventral telencephalon (vtel) and the diencephalon (black asterisk) display the expected loss of Ldb1 expression. D–F, Expression of Lhx2 mRNA and mTmG (GFP) reporter in E12.5 control (D), Emx1Cre;Lhx2lox/lox;mTmG (E), and NesCre;Lhx2lox/lox;mTmG (F) brains. Lhx2 is recombined and its expression is undetectable in the dorsal telencephalon of Emx1Cre;Lhx2lox/lox;mTmG brains, and mTmG reporter displays a complementary pattern, consistent with the activity domain for Emx1Cre (E). NesCre;Lhx2lox/lox;mTmG brains display no detectable Lhx2 expression and widespread expression of the mTmG reporter, consistent with the activity domain of NesCre (F). The control brains display autofluorescence in the green channel in the region of the choroid plexus which is an artifact. Scale bars: 100 μm.