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The ddm1 mutant was genetically identical to the wild type, except for the DDM1 locus and few other loci.
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These results demonstrated that a PL11 mutant is genetically stable.
The mutant was self-pollinated for several generations until the mutation was genetically proven to be truly inherited.
In previous studies, these phenotypically Pgm– or Ybt– spontaneous mutants were genetically undefined, or if defined were engineered in Y. pestis strains lacking virulence factors such as the pH6 antigen and YopJ, making it difficult to delineate the contribution to virulence of non-Ybt related genes within the pgm locus [5], [9], [10].
These independently isolated host range mutants were genetically repurified on E. coli K12 W3110 and were named: RB42 K1 and RB42 K2.
However, ribavirin-resistant mutants emerged when treated with low concentrations (≤0.2 mM) of ribavirin, and those mutants were genetically more stable during serial passages in cell culture.
Wif1 lacZ/lacZ mutants are genetically equivalent to the β-catenin GOF in urs, and perineal cleft phenotype of β-catenin GOF mutants are also observed in Wif1 lacZ/lacZ mutants.
The mutant phage was genetically modified [4], [5] to display a peptide extension of arbitrary sequence (Fig. 2).
The Otx1 mutant allele was genetically linked to MADM-11 GT through meiotic recombination.
For the generation of double mutants such as hy1 atmyc2, homozygous hy1 (WS) mutant plants were genetically crossed with atmyc2-1 (Col-0) homutantus mutant lines.
Since mice from each mutant strain are genetically identical and non-penetrance was usually unilateral, the phenotypic variability within each mutant strain likely results from stochastic molecular events.
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