Defects in Sensory Axon Growth Precede Neuronal Death in Brn3a-Deficient Mice

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

Fig. 1.
Fig. 1.

Brn3a 5′-flanking sequences target reporter gene expression to the sensory nervous system. A, Structure of the 5′-regulatory region of the mouse brn3a locus. Transcription is initiated from multiple closely spaced sites ∼300 bp upstream from the start of Brn3a translation. The positions of the previously identified distal and proximal autoregulatory sites are indicated (Trieu et al., 1999). Transgene constructs were produced by linking 6 or 11 kb of 5′-flanking sequence to the LacZ expression cassette at the Brn3a translational start site. B–D, The 11 kb/Brn3a transgenic construct targets LacZ expression specifically to the sensory system in E11.5, E12.5, and E14 mice, respectively. B and C show one of three transgenic lines that targeted LacZ specifically, and Dshows a second independent line. A third line is used for the experiments shown in subsequent figures. Arrows inD indicate areas of ectopic expression in the neuroepithelium of the forebrain and tegmentum that varied between transgenic lines.

  1. The Journal of Neuroscience vol. 21 no. 2 541-549
Responses to This Article
Be the first to respond to this article
Advertisement