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In a large-scale ENU mutagenesis screen for definitive hematopoietic mutations, we obtained cas002, a novel mutant with severe hematopoietic defects and recessive lethality.
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The fraction of mutants with severe deletions in the Hprt locus after exposure to oxygen ions increases from 65% at 60 keV/μm up to a maximum (100%) at 300 keV/μm and declines with higher LET values to 75% at 750 keV/μm.
In aux mutants with severe Notch-like mutant phenotypes, clathrin vesicle uncoating is inefficient.
Mutants with severe growth defects were eliminated from further analysis and the remaining potential biofilm mutants were reexamined for reproducibility in the biofilm assay.
However, the observation of a few cells with three TOs in the GDmg200 mutant indicates that this regulatory mechanism can be occasionally overcome in mutants with severe gliding deficiencies.
Mutants with severe defects in some sensory modalities displayed normal or nearly normal magnetic orientation.
Exocyst mutants with severe root growth defects have significantly reduced rates of elongation compared to Col-0 (p < 0.001, Potthoff analysis).
We found that the mutants with severe defects in the second antenna and appendage development have biallelic mutations, failed to molt, and died before becoming adults.
Homozygous exocyst mutants with severe root growth defects (i.e. sec8-1, sexo84b-1xo84b-1) are virtually sterile and were obtained in the progeny of self-crossed heterozygous plants.
Mature cortical cell lengths, primarily the result of cell elongation in the EZ, were indeed reduced in the mutants with severe growth defects.
Vps11, 16, 18 and 33 are class B Vps mutants with severe phenotypes – Vps11p/16p/18p/33p appears to be the core complex with Vps39p and 41p (class C mutants with milder phenotypes) providing accessory subunits and function [ 39].
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CEO of Professional Science Editing for Scientists @ prosciediting.com