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The phenotype of the ygl138 mutant was controlled by a single nuclear gene, which was tentatively designed as YGL138 t).
Genetic analysis revealed that phenotype of sug-h mutant was controlled by a complementary interaction of two recessive genes, OsBEIIa and OsISA1.
The segregation pattern was consistent with 1 3 ratio (χ2 = 0.62, P > 0.05), suggesting that the Al resistance and short root phenotype in ral1 mutant was controlled by a single recessive gene.
Quantitative RT-PCR analysis showed that the expression levels of known Al-resistance genes were not increased in the mutant compared to WT. Genetic analysis indicated that the Al-resistance phenotype in ral1 mutant was controlled by a single recessive gene mapped on the long arm of chromosome 6.
Because the GCAP1-Y99C mutant was controlled by a rhodopsin promoter in the transgenic mice and thus would not drive proper expression in cones, we limited our assays in this study to rod photoreceptors.
Prior to transcriptional analysis, the deletion of rsh in the Δ rsh mutant was controlled and confirmed by PCR using primers flanking the mutated region.
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To determine whether the soil-surface rooting and the lack of root gravitropic response observed in the mutant are controlled by the same gene, we performed segregation analyses by using 85 F2 plants derived from a cross between the mutant and WT Nipponbare (Table 1).
In these cells, expression of dominant negative mutants is controlled in a Tet-off system, i.e., absence of tetracycline results in dominant negative protein expression.
In addition, a cotton mutant, pag1, exhibited dwarfism due to significant inhibition of cell elongation and expansion, and brassinolide (BL) treatment rescued its growth and fiber elongation [ 6] These results indicate that most dwarf mutants are controlled by recessive genes, and involve very few dominant genes, and plant hormones play significant roles in plant height decision.
Comparison of expected and observed mutant count when the number of each mutant plaque was controlled for in each NGS library.
Genetic analyses indicated that the sug-h mutant phenotype was controlled by a complementary interaction of two recessive genes, Isoamylase1 (OsISA1), which was reported previously, and Starch branching enzyme IIa (OsBEIIa), which was newly identified in this study.
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