Therefore, it is likely that ubp2Δ mutants have a defect in internalization into MVBs.
In the second group, mutants have a typical defense defect in which bacterial growth is increased and survival is decreased.
This is only likely to occur in small populations where deleterious mutants have a chance to reach fixation.
Our findings indicate that DCM mutants have a deficit in force generation and force-holding capacity due to the reduced occupancy of the force-holding state.
bchs mutants have a reduced adult life span with the age-dependent formation of protein aggregates throughout the neuropil of the CNS.
Interestingly, nudt7 mutants have a lower GSH/GSSG ratio and therefore an altered redox state following infection, which may explain the enhanced resistance44.
However, recombinant human BChE and the known BChE mutants have a much shorter biological half-life compared to the native human BChE.
The egy1 deletion mutants have a yellow-green phenotype and reduced granal thylakoids.
The z3 2 and z3 3 mutants have a T-DNA insertion in the first exon, but in different locations.
From this, we determined that mtd1 1 mutants have a defect in gene-transfer through the male gametophyte (Table 2).
Deletion mutants of whi2 have an overgrowth phenotype when grown on low amino acid medium and this overgrowth is sensitive to the drug rapamycin, which indicates that whi2 deletion mutants have a defect in TORC1 regulation.
