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10.7554/eLife.06963.014 Figure 4. Overexpressing DMA-1 in ire-1 mutants can either rescue dendritic defects or cause more severe dendrite branching defects.

The diversity of physiological effects observed in luxS- mutants can either be interpreted as the result of a defect in a global quorum sensing regulatory mechanism, which may also be caused by a LuxS dependend compound other than AI-2, or as the result of a defect in the central methyl cycle of the cell.

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The fraction of mutants can increase either by mutant amplification (outgrowth of mutant cells) or by mutant enrichment (killing of susceptible cells).

For example, the haploid parental strain has an irregular shape whereas the mutants can be either circular and smooth (D1-n, SD1-n) or circular and rough (A2-n, A3-n, A4-n).

Mutant p53 can either inactivate wt p53 or complement mutant p53, depending of particular mutation.

Each mutant clone can either retain a fraction of the fitness neighbourhood of its parent, or obtain an entirely new fitness neighbourhood.

The mutant type can either have lower fitness than the wild type for all frequencies, or it can have a lower fitness only for small frequencies.

Mutants can be generated either using traditional methods such as gene deletion by homologous recombination or by using a transposon delivery vector.

If all genes of this p53 network are positively regulated by WT1Wilms3, we can conclude that the mutant WT1 protein can either enhance or antagonize the transcriptional activity of p53.

Those mutants can be classified as either functional, i.e. those with delayed overall senescence, or cosmetic, i.e. those where only chlorophyll degradation is delayed while other aspects of senescence progress normally [ 52].

By comparing expression of LHP1 targets in lif2, lhp1 and lif2 lhp1 mutants we showed that LIF2 can either antagonize or act with LHP1.

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