Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2009 Jan 12;184(1):101–112. doi: 10.1083/jcb.200805155

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2009 Wall et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

PMC Copyright notice

Figure 1. — Shh is required to maintain Hes1 protein and mRNA in postnatal retinal explants. (a) Diagram of the retinal explant culture method. Once the retina is surgically detached from the lens and surrounding ocular tissues, it is flattened by making four incisions and cultured on a membrane in the presence of a Smo agonist to activate the Hh signaling pathway. A cross section of a postnatal retinal explant is shown demonstrating Gli1 transcript expression in the Hh-responsive progenitor cells of the neuroblast region. The RGC layer is comprised of a population of postmitotic neurons that are not responsive to Hh signaling. Bar, 100 μm. (b) Retinal explants were treated with and without a Smo agonist at E14 (n = 3) and P0 (n = 3) for 3 d in culture and analyzed for Hes1, Hes5, and Gli1 mRNA by RT-qPCR. Values represent fold mRNA induction in Smo agonist–treated explants relative to untreated explants. Error bars represent SEM. *, P < 0.05. (c) Western blot for Hes1 from P0 retinal explants cultured for 3 d from untreated and Smo agonist–treated explants; β-tubulin protein level was used as a loading control.