FIGURE

Fig. 3

ID
ZDB-FIG-190723-1402
Publication
Pei et al., 2019 - AP endonuclease 1 (Apex1) influences brain development linking oxidative stress and DNA repair
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Fig. 3

Whole mount in situ hybridization demonstrates reduction in four key brain transcription factors after Apex1 knockdown in both wild-type and p53 mutant embryos with rescue by co-injection of mRNA for human <italic>APEX1</italic>.

Whole mount in situ hybridization shows aberrant distribution of critical brain markers after Apex1 knockdown. Rescue was achieved by co-injection of transcript for human APEX1. Similar results were obtained in p53 mutant embryos in which Apex1 was knocked down. Whole mount in situ hybridization was performed to examine fezf2, otx2, egr2a, and pax2a expression after knockdown of Apex1 in wild-type and p53 mutant embryos. Expression of each transcription factor decreased, and distribution was altered in both Apex1 MO injected wild-type and p53 mutant embryos, but was rescued by co-injection with human APEX1 capped mRNA. Note the small heads and eyes in Apex1 knockdown embryos. Hindbrain neurons (HBN) indicated by pax2a expression were no longer visible in Apex1 MO injected embryos (pax2a panel). Alteration in distribution or amount of signals is marked with arrows or brackets. KD knock down, WT wild-type, Res Apex1MO + human Apex1 rescue, p53m p53 mutant embryos, FB forebrain, MB midbrain, r5 hindbrain rhombomere 5, OS optic stalk, MHB midbrain-hindbrain boundary, OV otic vesicle. Whole mount in situ hybridization was performed with 20 embryos/group. All embryos are shown with anterior to the left
Expression Data
Genes:
Fish:
Knockdown Reagent:
Anatomical Terms: (all 6)
Stage: Prim-5

Expression Detail
Antibody Labeling
Phenotype Data
Fish:
Knockdown Reagent:
Observed In:
Stage: Prim-5

Phenotype Detail
Acknowledgments
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