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Both mutants failed to bind calcium.

Interestingly, both mutants fail to produce glycerol-induced spores (data not shown).

Both mph1 mutants failed to assemble significant levels of MCC-APC/C, and both failed to checkpoint arrest, highlighting the importance of Mph1 kinase activity in the spindle checkpoint.

Furthermore, both ca mutants failed to stimulate NF-κB as indicated by the luminescence reporter (Fig. 1F).

Parallel experiments with YFP-tagged PARK2 mutants demonstrated that both PARK2 mutants failed to translocate to mitochondria after FCCP treatment (Fig. 2F).

Surprisingly, while wild-type plants accumulated Raf in the leaves under all conditions tested, both RS5 mutants failed to do so in their leaves (Table  2) suggesting that At5g40390 is the only RS, in leaves, responsible for abiotic stress-induced Raf accumulation.

Consistently, both of these pUL31 mutants failed to bind to pUL34-GUVs.

Both T184A and T188A mutants failed to be autophosphorylated even with prolonged phosphorylation time.

For two mutants, or990 ts and or1247 ts, a different mis-sense mutation was found in the same gene in both mutants; this was the only candidate gene shared by both mutants, and the two mutants failed to complement each other (Table S1).

However, both Tim9 mutant complexes were sensitive to trypsin digestion, as the mutants failed to protect both themselves and WT Tim10 from degradation.

In contrast, both of the N185D and S156A mutants failed to induce any significant cell invasion in either BEAS-2B cells or NIH3T3 cells compared with mock.