Unexpectedly, the I134F mutant was unable to turn over but could initiate and partially elongate the polyketide chain.
The NK41 mutant was unable to induce a pro-inflammatory response and to damage the invaded human respiratory epithelial cells.
As observed following disruption of the Saccharomyces cerevisiae ortholog, HMX1, a CaHMX1 null mutant was unable to grow under iron restriction.
This mutant was unable to bind MreC in conditions where wild-type PBP2 could generate a stable complex in gel filtration (Supplementary Fig. 2).
Under non-growing conditions in phosphate buffer, a mucoid clinical strain formed microcolonies on steel surfaces, while an acetylation-defective mutant was unable to form cell clusters.
The mutant was unable to colonize mouse organs following infection.
Furthermore, a Newman sigB mutant was unable to survive phagocytosis, with all ingested bacteria killed within 2 days (Fig. 6C).
In addition, the K51A mutant was unable to form homodimers in the Venus fluorescence complementation assay (figure S5).
Remarkably, the K48-only ubiquitin mutant was unable to form aggregates, in agreement with a requirement for K63 (Fig. 2E).
Actually, the TolC defective mutant was unable to multiply within host cells from the early steps of host invasion.
Finally, the mutant was unable to transactivate the GRE2-Luc reporter gene in the absence or presence of hormone (Fig. 3E).
