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The trimer stability of an AcrB mutant needs to reach a threshold value for the protein to display activity.
3) The result with the mec1∆ tel1∆ double mutant needs to be reported in order to conclude that the DNA damage checkpoint is not required for stopping transcription around a DNA double strand break.
This is not surprising since k3 sets the strength of the signal from the bound CLV1 receptor and the loss-of-signal mutant needs to be able to reduce this signaling strength for the clv1-1 mutant.
The data regarding loss of transcription around the DSB at the LEU2 and ARG5,6 loci are reported in the new Figure 3. 3) The result with the mec1∆ tel1∆ double mutant needs to be reported in order to conclude that the DNA damage checkpoint is not required for stopping transcription around a DNA double strand break.
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This synthesis is intended to provide a useful source of reference when studying the molecular controls of hair follicle growth and differentiation, and whenever the hair phenotypes of a newly generated mouse mutant need to be compared with existing ones.
Therefore, the flux distributions for a mutant need to be simulated for all combinations of the enzymes with measured activities.
Particularly, the possibility of feedback inhibition of thiamine biosynthetic (nmt1 + and nmt2 +) and transport (bsu1 +) genes by thiamine in the Δphx1 mutant needed to be evaluated.
Since we found the unique expression of SEMA3C in the limb (Fig. 2A), lymphatic vessel development in Sema3c mutants needs to be investigated.
To evaluate the mechanisms regulating seed length, observation of microtubule arrangement and analysis of double mutants among srs1, srs3, Srs5, and various BR mutants need to be performed.
Ideally, complete loss-of-function mutants need to dispose of entire coding sequences.
Therefore, studies with the maize bm mutants need to be done with near-isogenic lines.
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