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Figure 7
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Figure 7
Figure 7. Slc38a9 deficiency leads to dysregulated hypoxia response. (A) The FPKM of hypoxia-induced genes in WT and slc38a9 mutant zebrafish embryos (60 hpf). (B) The phenotypic penetrance of the slc38a9 mutant increased under hypoxia treatment. Zebrafish larvae (24 hpf) were treated with hypoxia embryo rearing solution (DO = 1 mg/L) for 10 h. Normoxia (Nor) and hypoxia (Hyp). (C) The hypoxia-induced increase of Hif1α target genes was blocked in the slc38a9 mutant zebrafish. The experimental groups were the same as described in (B). The expression of Hif1α target genes was detected by qRT-qPCR and normalized by the β-actin mRNA levels. The mRNA levels of Hif1α target genes were upregulated in WT zebrafish larvae under hypoxic conditions, while this increase was completely blocked in the slc38a9 mutant. Data shown are mean ± SEM, n = 3. * p < 0.05, ** p < 0.01, *** p < 0.005, **** p < 0.001. (D) The increase of Hif1α protein level was attenuated in slc38a9 mutants under hypoxic conditions. The experimental groups were the same as described in (B). The immunoprecipitation was used to enrich the Hif1α protein. The representative result is shown in (D). > Hif1α.
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Full text @ Int. J. Mol. Sci.