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Two Ser mutants were unable to grow anaerobically on fumarate, nitrate or nitrite.
Additionally, the mutants were unable to distinguish between rough and smooth textures.
Two other Ser mutants were unable to grow anaerobically on all compounds tested as sole terminal electron acceptor.
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.
It is likely that ΔscrA and ΔscrAΔscrB use the complex carbon source for growth even in the presence of high concentration of sucrose since these mutants were unable of transporting sucrose into cell.
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).
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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].
We confirmed that gB null mutants are unable to spread from neurons to cells in our chamber.
Out mutants are unable to cause maceration symptoms [7] and mutants affected in the Prt secretion system are delayed in symptom progression [8].
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