In conclusion, the error-threshold exists for high lethality of mutants also in the finite population model.
Siderophore excretion in the mutant also decreased in iron-depleted medium.
Expression of Abl in a fra mutant also results in dozens of axons exiting toward the periphery (AEP defects), and, surprisingly, this defect is readily observed using BP102.
Overexpressing TcLAR in Arabidopsis ldox mutant also resulted in elevated synthesis of not only catechin but also epicatechin.
As shown in Figure 3A, 32D cells expressing the K762R/G-CSFR mutant also hyperproliferated in response to G-CSF compared to WT G-CSFR transfectants.
The hda1Δ/Δ mutant also filamented in all media tested, but the filaments of the hda1Δ/Δ mutant appeared shorter than wild-type.
32Dcl3 cells stably expressing the K762R/G-CSFR mutant also hyperproliferated in response to G-CSF and exhibited enhanced survival following cytokine depletion.
This subnuclear phenotype contrasted with that of a ddm1 mutant also deficient in centromeric CG methylation, which more closely resembled the wild type centromere organization.
In addition, some other genes found in rice mutant also play key roles in controlling leaf rolling.
Apparently, the YnaIΔ2−63 mutant also opens spontaneously in KNO3 solutions.
