Hnrnpa1a and Hnrnpa1b single KO fish do not show a phenotype due to functional compensation. (A)hnrnpa−/− single mutants show no obvious morphological phenotype. Images of 5 dpf old wildtype, hnrnpa1a−/−, hnrnpa1b−/− and hnrnpa3−/− mutants. Lateral view. Anterior to the left. Images were taken with Axio Scope A1. (B) Hnrnpa1a and Hnrnpa1b but not Hnrnpa3 compensate for each other’s loss. mRNA levels of hnrnpa1a were significantly upregulated in brains of hnrnpa1b−/− (***p < 0.0001; n = 4) and hnrnpa3−/− (***p < 0.0001; n = 4) mutants. Normalized to rflp13a and elf1a2. Error bar indicates SEM. Unpaired t-test. Results by qRT-PCR were reproduced twice using the same cDNA. (C) Hnrnpa1b levels were significantly upregulated in brains of hnrnpa1a−/− mutants (hnrnpa1amde13: **p < 0.001, n = 8; hnrnpa1amde14: ***p < 0.0001, n = 8) and not changed in brains of hnrnpa3−/− mutants (p > 0.69, n = 4) compared to their wildtype siblings. Hnrnpa3 levels were not changed in brains of hnrnpa1a−/− mutants (p > 1.1, n = 8) and hnrnpa1b−/− mutants (p > 0.64, n = 8) compared to their wildtype siblings. Student’s t-test. Error bars indicate S.E.M. Calnexin served as a loading control. Statistical significance was defined as p < 0.05. n.s., not significant.
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