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The results are consistent with an autosomal dominant mutant causing the white phenotype.
It appears that Na+ ions can substitute for protons and bind to the counterion in the initial state of the D251E mutant, causing the red shift of the absorption spectrum.
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The prolonged vegetative phase in the mutant caused the panicle length and primary branch number of ghd10 to increase under natural SD conditions compared with the wild type (Figure 1D, E).
Hence, it was proposed that the upregulated expression of maternal PHE1 in the mea mutant causes the endosperm and embryo of mea seeds to overproliferate after fertilization and eventually abort [42, 43].
Also, MVI depletion or overexpression of H246R mutant caused the formation of significantly wider or aberrant myotubes, respectively, indicative of involvement of MVI in myoblast differentiation.
Chromatin immunoprecipitation (ChIP) experiments performed with antibodies specific for H3K9Ac revealed that H3K9Ac levels are elevated on subtelomeric sequences in cells lacking sir2, and that the sir2N247A mutant causes the same enrichment of H3K9Ac as does loss of sir2.
However, it is unlikely that the restoration of Cbl binding in the Y1045+ mutant caused the partial rescue of CME through EGFR ubiquitination, since the EGF dose response of CME of this mutant was rather different from that of its ubiquitination, while the dose response of its NCE was congruent with it (Supplementary Figure 12B).
Based on our mechanical fractionation study and secretion assay it is tempting to speculate that the interactions between EvpC and EvpI might be disrupted in these mutants causing the abolition of secretion.
Proinsulin mutants causing the MIDY syndrome are distinct both from insulinopathies previously described as associated with adult onset-associated diabetes [3] and from recessive alleles that result in neonatal diabetes through reduced insulin expression [18].
These observations suggest that the reduced levels of Pio accumulation in the tracheal lumen in γCOP mutants cause the disruption of dorsal branches.
Thus, miRNA mutants cause the inflorescence transcriptome to resemble leaf and meristem transcriptomes and to diverge from pollen and seed transcriptomes.
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