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We tested the function of the light-responsive circadian clock in the vvd mutant and found no major defect in the circadian rhythm of conidiation or light regulation of a key clock component, frequency (frq).
We also overexpressed the NRT1.1 in the nlp7-4 mutand and found that the YFP signal, nitrate content, nitrate reductase activity, and the induction levels of the endogenous genes after nitrate treatment in the NRT1.1/nlp7-4 NRT1.1/nlp7-4omplantsy or partially recovered to wereevels (Fig. 3).
We compared the 528 differentially expressed genes in the nlp7-4 mutand and 485 differentially expressed genes in the chl1-13 mutand and found 342 genes (64.8% of 528 and 70.5% of 485) were regulated by both NLP7 and NRT1.1 (Fig. 4, Supplementary Dataset 3) while 143 and 186 genes were regulated only by NRT1.1 and NLP7, respectively (Fig. 4, Supplementary Dataset 4).
We measured cAMP levels in the ΔfimL mutant and found decreased levels of cAMP, similar to the diminished levels observed in ΔcyaB.
Accordingly, we designed and constructed a RIG-I Q299A mutant, and found that the mutated protein is unable to bind significantly to biotinylated leader RNA (Figure 5G).
The current study investigated the genetic, physiological, and morphological characteristics of a newly discovered lepidopteran melanic larval mutant and found no evidence that JH, nor melanin granules, are involved in producing the melanic phenotype.
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In addition, we synthesized a miR-29a mutant that restores complementary to the mutant miREs and found that this mutant miRNA successfully restores repression of the PTC -APC mRNA bearing mutant miREs.
We then created tt2-5 sk11 sk12 triple mutants, and found that tt2-5 completely suppressed sk11 sk12 phenotypes pertaining to seed coat color (Fig. 3f) and fatty acid levels (Fig. 3g, left panel).
We constructed MC159 truncation mutants and found that the amino-terminal region before the first DED and nearly all the carboxyl terminus after the second DED were dispensable for the antiapoptotic activity of MC159.
Using an assay developed by us previously21, we quantified the frequency of emergence of phage resistant mutants, and found that growth in LB supplemented with spent medium containing autoinducers caused the emergence of phage resistant derivatives of the target bacterium at an enhanced rate as compared to a culture without added autoinducer preparations (Fig. 4).
Having established that ephrinB2 can associate with TBC1d24, we expressed TBC1d24 in the embryos along with ephrinB2 deletion mutants and found that deletion of six amino acids in the C-terminus encompassing the PDZ-binding motif markedly reduced the interaction with TBC1d24 (Fig. 1b).
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com