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. 2005 May 4;25(18):4540–4549. doi: 10.1523/JNEUROSCI.0492-05.2005

Figure 1.

Figure 1.

Increase in Edn2 transcript abundance in diverse mouse models of photoreceptor disease. A, Scatter plot comparing the ratio of prCAD-/-/WT retina RNA hybridization signals in two independent microarray experiments. Hybridizations were performed with the Affymetrix mouse genome MOE430 chip, and the ratios are plotted on a log2 scale. Points representing Prcad, Edn2, and noncoding transcript AK018172 are labeled. As expected, the transcript with the greatest reduction in abundance in the prCAD-/- retina is that coding for prCAD itself. B, RNA blot showing Edn2 transcripts in WT, prCAD-/-, rds-/-, and rd7 retinas. Arrows to the right of this and subsequent blots indicate the high abundance ∼4.5 kb and the lower abundance ∼1.4 kb Edn2 transcripts. Probing the blot with Gapdh in this and all subsequent RNA blots controls for equal loading of RNA. C, In situ hybridization showing the accumulation of Edn2 transcripts in photoreceptor cells in prCAD-/-, rds-/-, and rd7 retinas. Specific Edn2 hybridization is undetectable in the control WT retina (left). In the rd7 retina, Edn2 transcripts accumulate only at the sites of retinal detachment (vertical arrows). ONL, Outer nuclear layer.