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Thus, miRNA mutants cause the inflorescence transcriptome to resemble leaf and meristem transcriptomes and to diverge from pollen and seed transcriptomes.
These observations suggest that the reduced levels of Pio accumulation in the tracheal lumen in γCOP mutants cause the disruption of dorsal branches.
Overexpression of α-Syn, through its gene duplication and triplication, is linked to idiopathic Parkinson's disease (PD), while its A30P and A53T mutants cause the autosomal dominant forms of familial PD [2] [4].
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Since Baz is essential for proper targeting of Crb and AJ [6], [7], mispositioned Baz in cnn mutants causes the defects of Crb and AJ (Figure 4B).
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].
Similarly to the wild type variant of vimentin these mutants caused the decreased mitochondrial motility (Fig. 5).
Several mutants caused the formation of chromatin bridges between mitotic nuclei (Fig. 5B), as seen when embryos develop without detectable Xpd (Li et al., 2010).
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].
The results are consistent with an autosomal dominant mutant causing the white phenotype.
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