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The kidney tissue sections from transgenic founders, chimeric mice with wild type HNF-1β and HNF-1β deletion mutant, were stained with collectrin antibody (red) and V5 antibody (green) (Figure 1d) and nuclei were counterstained blue with 4'-6-diamidino-2-phenylindole.

Pollen grains in the WT and GMS mutant were stained with 2% I2-KI to detect starch activity at 0 DPA.

The pollen grains in the WT and the mutant were stained with 2% I2-KI to detect starch activity during the flowering period.

Approximately 4% of small buds of the chs2Δ chs8Δ mutant were stained with PI indicating that death occurred during early polarized growth in these cells (Fig. 1A,B and Table 2).

When using the mutant-specific G127X Ra 123 132 SOD1 ab, approximately 25% of the glial cell nuclei in both FALS patients with the G127X SOD1 mutant were stained, whereas using the Chi 131 153 ab, (raised to a peptide sequence that is absent in the G127X-mutated SOD1 protein) also gave staining of misfolded SOD1 in glial cell nuclei in the G127X patients.

Non-transfected PC12 cells (NT) and cells transfected with either wild type human ZnT3-myc or ZnT3 tyrosine mutants were stained with zinquin (Fig. 5C).

Controls and mutants were stained simultaneously using the same solutions, in the same Eppendorf tubes or glass vials, and imaged on the same days using identical microscope settings.

Very similar images of stretched kinetochores were also observed when the mutants were stained for tagged versions of various other kinetochore proteins such as CENP-CCnp3, Mis12, Nuf2, and Sim4 (data not shown, and below).

To measure mitochondrial superoxides, cells overexpressing Magmas and Magmas mutants were stained with 25  μM MitoSOX for 15 min and mounted in ProLong Gold Antifade reagent with DAPI (Invitrogen).

The wild type, fat-5, fat-6 and fat-7 mutants, as well as fat-5 fat-6 and fat-5 fat-6 double mutands were stained with both the vital dye Nile Red and with the fat-5 fat-7e Oil Red-O, both ofat-5 fat-7e previously been usedoubleharacterize fat storage in C. elegans [ 12, 21].

DOI: http://dx.doi.org/10.7554/eLife.07074.010 To confirm that the phenotypic basis of the selective advantage is similar to the previously described WS mutants (where activation of a DGC results in overproduction of cellulose [ McDonald et al., 2009]) reconstructed mutants were stained with calcofluor and Congo red and their colony morphology examined.