This mutant cannot form normal appressoria and is therefore unable to penetrate rice or barley leaves.
We showed previously that under non-permissive conditions this degron mutant cannot form colonies from single cells, exhibits a strong reduction in doubling time within 2 h, and essentially ceases growth and division by 8 h after the shift to non-permissive conditions.
In contrast, csf1ra mutant zebrafish cannot form a complete non-sex-specific stripe pattern (Parichy et al. 2000a; Parichy and Turner 2003b).
Furthermore, incubation of p66CH2CB WT or p66CH2CB-Cys59Ser with Prx1-Cys83Ser, a Cys83Ser regulatory mutant that cannot form higher Prx1 oligomers but exists only as a dimer, also results in this dominant band.
Furthermore, with a quantitative bifluorescence complementation (BiFC) assay, we found that the resting BCR forms stable dimers on the cell surface while a BCR mutant that cannot form dimers is hyperactive and cannot be stably expressed on the B cell surface (Yang and Reth, 2010b).
The within-dimer BtubB mutant, in contrast, cannot form a dimer with wild type BtubA.
We also showed that a mutant BCR that cannot form a BCR oligomer is hardly expressed on the cell surface.
After fertilization, the first two centrioles are observed via the recruitment of the zygotic PCM proteins and are seen in asterless mutant embryos that cannot form centrioles.
Mutants 1 and 2 cannot form the hypothesized PK and are less resistant to the Xrn1 than WT, but to only a moderate extent (64% and 88% resistance of WT, respectively).
