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Strong, ubiquitous overexpression of parkin in vps35 mutants was unable to rescue these phenotypes (data not shown).
Pollen from polyamine oxidase (PAO) mutants was unable to cause the opening of Ca2+-permeable channels in the presence of spermidine, which resulted in reduced pollen tube growth and seed number.
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Two Ser mutants were unable to grow anaerobically on fumarate, nitrate or nitrite.
Two other Ser mutants were unable to grow anaerobically on all compounds tested as sole terminal electron acceptor.
Additionally, the mutants were unable to distinguish between rough and smooth textures.
A CNOT7 K203A mutant abrogates the interaction with Tob (Horiuchi et al., 2009), while BTG2 W103andnD105A5A mutants were unable to interact with CNOT7 (Yang et al., 2008).
However, Δefg1 and Δcph1/Δefg1 mutants were unable to filament and did not form biofilms, but rather sparse monolayers of loosely attached elongated, rod-like, cells.
BvrR/bvrS mutants are unable to multiply intracellularly and are avirulent in the mouse model [4].
che-1 mutants are unable to chemotax to NaCl yet show wild-type chemotaxis to NH4Ac.
In many species, ppk mutants are unable to survive during stationary phase [55].
However, all single septin mutants were unable to grow in solid medium at 34°C (Fig. 3A).
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