Surprisingly, unlike D. discoideum acra-, the P. pallidum acra- mutant displayed normal spore formation in fruiting bodes (Figure 3A,B).
The hrk1Δ mutant displayed normal levels of capsule production comparable to the wild-type strain, whereas the hog1Δ mutant showed increased capsule production as previously described [5], [6], [8].
However, since our cheR1 mutant displayed normal swarming motility on 0.5% agar plates, we rather hypothesize that chemotaxis driven swimming motility is necessary for formation of mature biofilm structures.
We identified Ser, but not Ser, as a PCTAIRE-1-dependent phosphorylation site; however, contrary to our hypothesis, phospho-deficient S336A mutant displayed normal binding to PCTAIRE-1.
Monitoring phosphorylation of Ser may provide a useful read-out to assess cellular activity of PCTAIRE-1 in vivo; however, a phospho-deficient S336A mutant displayed normal interaction with PCTAIRE-1.
The Tgfβ2−/− Tgfβ3−/− double knockout mice and Tgfβ2−/− Tgfβ3+/− mutants show VBWD, whereas Tgfβ2+/− Tgfβ3−/− mutants display normal ventral body wall fusion.
Therefore, it allows a simple assay to assess metabolic alterations introduced by mutagenesis: mutants displaying normal growth in the presence of cerulenin are good candidates to be high-lipid producers due to their ability to overcome this inhibition.
lov1 mutants displayed normal responses to phytohormones and most of the abiotic stresses (data not shown).
In addition, they had a variable rough eye phenotype because of irregular ommatidia (compare Figure 4D F), while the viable BicDA40V, S103A and BicDA40V, S103F mutants displayed normal eyes (Figure 4G and H, respectively).
