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While the root tip including root cap, meristem and transition zones was heavily stained in the wild-type, the mutant displayed much lighter color in the root tip (Fig. 5a), indicating that ral1 mutant accumulated less Al in root tips than WT.

Intriguingly, both wild-type synphilin-1 and the R621C mutant displayed much higher capacities for inclusion formation than α-Syn and we believe that this directly relates to our observation that synphilin-1 is a true lipid raft interactor in both yeast and mammalian cells, while α-Syn associates only poorly with these membrane domains, as previously shown [13], [31].

No such growth defects were observed in the imeBΔ, mpkCΔ, phoAΔ, and phoBΔ mutants but the imeBΔ mutant displayed much denser hyphae due to stronger growth on media containing protein (BSA) as a nitrogen source, similar to the xprG1 and hxkDΔ mutants.

A trypsin digestion assay was performed, and the mutants displayed much higher stability against trypsin hydrolysis compared to the native enzyme.

Immunohistochemical evaluation of pancreata from Hq mutant mice displayed much smaller islets compared to wild-type mice (WT).

However, the non-polar mutant strain displayed much lower nitrogenase activity than the wild type strain under nitrogen fixation conditions (0.1 mM ammonium and 0.5% oxygen tension), suggesting that PnfA is necessary for maximal nitrogenase activity.

The ceh-20; unc-62 double mutant, strain AW679, displayed much more extensive seam hyperplasia, up to 70 seam cells per side, extending throughout the length of the animal (Fig. 2), suggesting that CEH-20 and UNC-62 interact in a complex to control the correct development of the seam lineage.

TP53-mutant Daoy cells displayed much higher levels of TAp73 and of total ΔNp73 RNA (9-fold ± 1 (mean ± S.E.M).

With 240 uM iron chelator, the fur mutant displayed a much shorter lag phase than MR-1 and reached a higher cell density at stationary phase, suggesting that the fur mutant better tolerated the iron depletion stress.

Surprisingly, all nrdAB mutants overexpressing nrdHIEF proved capable of growing in the presence of oxygen with only a class Ib enzyme, although they displayed much slower growth rates as well as a filamentous morphology (Figure S2).

In line with these results, INZ displayed much higher toxicity to p53-containing human cancer cells compared with WI-38 and NHF, or p53-mutant and null cancer cells.