A genetic mutation led to lighter fur, and the sandhills mice lucky enough to be born mutants were more likely to survive and breed.
For thermotolerance, several mutants were more heat tolerant than their wild-type parents.
Moreover, M6 and M10, which are biofilm mutants, were more susceptible to N3-8 than N2-4.
As seen with the 111In-labelled mutants at 48 h post injection, tumour-to-blood ratios for 131I-labelled mutants were more favourable than wild type (Table 3).
Isolated cardiomyocytes from conditional mutants were more susceptible to anthracycline toxicity, demonstrating that ErbB2 signaling in cardiomyocytes is requisite for the prevention of dilated cardiomyopathy (DCM) [14].
For instance, the mutants unable to produce trehalose (i.e., the Δtps1Δtps2 and Δtps1Δhxk2 mutants) were more sensitive to osmotic stress than the wild-type strain (Hounsa et al. 1998).
In contrast, the weak-catalytic-activity mutants were more sensitive to the cytotoxicity of BPDE and UV-C than the wild-type cells, and displayed much higher sensitivity to the clastogenicity of BPDE than the wild-type cells in an in vitro micronucleus assay.
These mutants were more carefully examined for sensitivities to HU and CPT.
The result (Fig. 4B) showed that the ΔmelC mutants were more resistant to catechol.
As shown in Figure 8C, all three mutants were more sensitive to lysis by SDS.
As shown in Figure 7, the color mutants were more pathogenic to the insect than the wild type strain Af293.
