Figure 6.
BCAS2 deprivation triggers alternative splicing of Mdm4 without gross changes in DNA damage. (A) The expression of γH2AX in bcas2−/− embryos and siblings showed no difference, even under UV treatment. (B) Semiquantitative PCR analysis and relative quantification of total Mdm4-FL and Mdm4-S isoforms in the CHT region of siblings and bcas2−/− mutants. (C) Sequencing of the shorter product showed a deficiency of exon 6 compared with Mdm4-FL. (D) Real-time PCR analysis of total Mdm4-FL and Mdm4-S isoforms in the CHT region of siblings and bcas2−/− mutants. (E) Mdm4-FL protein levels are reduced in bcas2−/− embryos that can be recovered by re-expression of bcas2. (F-I) Ectopic expression of wild-type bcas2 mRNA can rescue HSPC defects in bcas2−/− mutants at 4 dpf. Scale bars, 200 μm.

BCAS2 deprivation triggers alternative splicing of Mdm4 without gross changes in DNA damage. (A) The expression of γH2AX in bcas2−/− embryos and siblings showed no difference, even under UV treatment. (B) Semiquantitative PCR analysis and relative quantification of total Mdm4-FL and Mdm4-S isoforms in the CHT region of siblings and bcas2−/− mutants. (C) Sequencing of the shorter product showed a deficiency of exon 6 compared with Mdm4-FL. (D) Real-time PCR analysis of total Mdm4-FL and Mdm4-S isoforms in the CHT region of siblings and bcas2−/− mutants. (E) Mdm4-FL protein levels are reduced in bcas2−/− embryos that can be recovered by re-expression of bcas2. (F-I) Ectopic expression of wild-type bcas2 mRNA can rescue HSPC defects in bcas2−/− mutants at 4 dpf. Scale bars, 200 μm.

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