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In contrast to the phoP mutant, the two pmr mutants were fully virulent, producing severe diarrhea (Figure 7A), multiplying in the colon, and spreading systemically (Figure 7B).

Moreover, these defective phenotypes could not be found among the rescue flies (Table 4), indicating that the defective phenotypes in the mutants were fully rescued.

Myc-COMMD1 and Myc-COMMD1ΔCOMM mutants were constructed using the Gene-Editor kit (Promega) and the resulting mutants were fully sequenced.

Previous studies have reported that the prfA* mutants with mid-level PrfA activity (prfA G155S mutants) were fully virulent when intravenously inoculated into mice based on the bacterial CFU required for a 50% lethal dose (LD50) [32].

In 1994, for example, IR-sensitive D. radiodurans polA mutants were fully complemented by expression of the polA gene from the IR-sensitive E. coli [4]; and in 1996, UV-sensitve D. radiodurans uvrA mutants were complemented by uvrA from E. coli [90], suggesting that these recombination and excision repair genes are necessary but not sufficient to produce extreme DNA damage resistance.

The resulting mutants were fully sequenced to confirm the sequence change.

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Paradoxically, however, IR-, UV-, and mitomycin-C (MMC -sensitive D. radiodurans polA MMC -sensitivelly complementeD.by expradioduransthe polA gene fromutantsR-sensitive Escherichiareoli [4].

For TPK2 and CKA2, the role in virulence appears to depend on the murine infection model used, as the respective deletion mutants are fully virulent in murine systemic candidiasis, but attenuated in oropharyngeal candidiasis and epithelial cell models [38], [39], [40].

WHIRLY mutants have a low penetrance of chlorotic variegation, and these mutants are fully autotrophic.

Cells that do not carry a chromosome inversion were tested first, showing that dinG uvrD and dinG rep double mutants are fully viable.

The early flowering phenotype of flc-2 mutants was fully rescued in transgenic lines, demonstrating that the fusion proteins are functional.

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