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. Author manuscript; available in PMC: 2020 Jun 15.
Published in final edited form as: Genet Med. 2020 Feb 27;22(6):1040–1050. doi: 10.1038/s41436-020-0758-9

Figure 4. Exoc7 is essential for zebrafish telencephalon development.

Figure 4.

(A) Exoc7 amino acid sequence is highly conserved between human, mice, and zebrafish. (B) exoc7 1bp frameshift deletion mutation in exon 5 is confirmed by DNA sequencing and predicted to cause a frame shift and subsequently a protein truncation through a premature STOP codon at amino acid 186. (C) exoc7 homozygous mutant fish have gross developmental abnormalities by 5 dpf notably small eyes and head edema. Green line shows measurement of adjusted head diameter calculated by subtracting edema (red lines). (D) Heterozygous exoc7 zebrafish crosses generated mutant fish (small eye/edema or dead) at expected Mendelian ratio. Genotyping confirmed that phenotypically mutant larvae were homozygous for the exoc7 mutation. (E) Quantification of adjusted head diameter, which is significantly reduced in homozygous mutant fish. (F) Body length is not significantly changed in homozygous mutant fish. (G) Toluidine blue stain of 5 dpf wild-type and exoc7 mutant zebrafish. (H) Apoptag staining shows a significant increase of apoptotic cells in the exoc7 mutant telencephalon. (I) Immunohistochemical staining of neuronal progenitors using Sox2. The number of Sox2+ progenitors is significantly decreased in the exoc7 mutant telencephalon. P-values calculated with two-tailed t-test. Error bars represent SEM.