FIGURE

Fig. 4

ID

ZDB-FIG-120301-42

Publication

Wan et al., 2012 - HB-EGF Is Necessary and Sufficient for Müller Glia Dedifferentiation and Retina Regeneration

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Fig. 4

HB-EGF and Ascl1a Regulate Notch-Signaling Component Genes in the Injured Retina (A) Real-time PCR shows injury-dependent induction of Notch-signaling components. (B) RT-PCR shows that HB-EGF activates Notch-signaling component genes in the uninjured retina. (C) RT-PCR shows that MO-mediated HB-EGF_a knockdown suppresses injury-dependent induction of Notch-signaling component genes. (D) Real-time PCR quantification of (C). ^*p < 0.01. (E) RT-PCR shows that Ascl1a knockdown suppresses injury-dependent induction of Notch-signaling component genes. (F) Real-time PCR quantification of (E). ^*p < 0.01. (G) Ascl1a knockdown suppresses HB-EGF-dependent induction of notch1 and her4 mRNAs. Arrows identify notch1 and her4 mRNA expression in control MO-treated cells. Scale bar, 50 μm. Error bars represent SD. ONL, outer nuclear layer; INL, inner nuclear layer; GCL, ganglion cell layer. See also Figures S4 and S5.

Expression Data

Genes:	dla dlb dlc dld notch1a
Fish:	WT WT + MO1-ascl1a WT + MO1-hbegfa WT + MO2-ascl1a
Condition:	physical alteration: anatomical structure
Knockdown Reagents:	MO1-ascl1a MO1-hbegfa MO2-ascl1a
Anatomical Term:	retina
Stage:	Adult

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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Reprinted from Developmental Cell, 22(2), Wan, J., Ramachandran, R., and Goldman, D., HB-EGF Is Necessary and Sufficient for Müller Glia Dedifferentiation and Retina Regeneration, 334-347, Copyright (2012) with permission from Elsevier. Full text @ Dev. Cell