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Double mutant analysis indicated that SRL2 and SLL1/RL9 function in different ways to regulate abaxial-side leaf development (Liu et al. 2016).
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Double mutant analysis indicates that Gli3 repressor activity is normal in hnn embryos, but Gli activators are constitutively active at low levels.
Thus, the mutant analysis indicates that BicD's role in balancing plus-end versus minus-end motion is functionally separable from its role in facilitating overall upregulation of transport, with the resulting long runs in each direction in Phase IIB (Fig. 6H, I).
Mutant analysis indicates that Dga1 contributes more significantly to TAG synthesis in the stationary phase, whereas Lro1 apparently is more active during logarithmic growth (Oelkers et al. 2002).
Double mutant analysis indicates a possible synergistic interaction between svr3 and svr7, which is defective in a chloroplast pentatricopeptide repeat (PPR) protein.
While our findings indicate that the expression of otd is relatively low compared to the level of ems expression in the ALl1 neuroblast, our mutant analysis indicates that otd is essential for the development of the neurons in this lineage.
We are currently unable to define where in the pathway this effect is occurring, though our mutant analysis indicates differences in the sensitivity of interfering and non-interfering repair to sequence polymorphism.
In case of Δ vvd, both the enrichment of carbohydrate metabolism genes, as well as the beneficial effect of several genes on cellulose degradation, as revealed by mutant analysis, indicate that the reason for enhanced cellulose degradation by the Δ vvd mutant lies at least in part in increased expression level of hydrolytic enzymes.
Mutant analysis indicates that a transcriptional network centered on the transcription factor NANOG marks and defines the Epi fate (Chambers et al., 2007; Frankenberg et al., 2011), whereas a network centered on GATA transcription factors underlies the PrE fate (Bessonnard et al., 2014; Schrode et al., 2014).
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.
Further MSD analysis indicated that the mutant is about 20-fold more diffusive than the wild-type motor in the no nucleotide state (D = 0.01 ± 0.0006 μm/s vs 0.00045 ± 0.00011 μm/s) and about 30-fold more diffusive in the AMPPNP state (D = 0.0036 ± 0.00011 μm/s vs 0.00011 ± 0.00001 μm/s).
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