Sentence examples for mutants to develop from inspiring English sources

It is also possible that one or both of these other EF-G genes can contribute to protein synthesis during later stages of plant development, which could allow the sco1-1 and sco1-4 mutonts to develop green leaves.

The o-vanillin plus fludioxonil pairing did not allow these mutants to develop tolerance to fludioxonil, resulting in 100% mortality.

While mature chloroplasts of fln mutants fail to develop properly and mutants have severe growth defects in the light, cell elongation in the dark is largely unaffected.

crc knockout mutants fail to develop nectaries, whereas bop1/bop2 double mutant lines have significantly smaller nectaries along with aberrant morphologies [ 26, 29].

Longitudinal hand sections of mature mutant kernels showed both reduced endosperm development as well as embryo defects, with most mutants failing to develop embryonic roots or leaves.

The occurrence of these phenotypes was dependent upon intact EPIYA motifs, as phosphorylation-resistant mutants failed to develop disease in the same experimental settings [ 146].

Scx has an established role in later stages of epiblast maturation: from around E6.5 the epiblast of Scx mutants fails to develop further and does not properly epithelialize.

Extra-embryonic structures derived from proximal streak mesoderm (chorion, allantois, yolk sac blood islands), and distal streak mesoderm (notochord, foregut, cardiac mesoderm) in amn mutants appear to develop normally, but embryos have impaired assembly of derivatives of the middle primitive streak, resulting in the absence of paraxial, intermediate and lateral plate mesoderm.

Furthermore, a proportion of mutants failed to develop a full response for a number of specific reflexes, i.e. those assessed via crossed extensor (5/11 animals failed), negative geotaxis (3/11), cliff avoidance (4/11), bar holding ability (11/11) and rotarod (7/11) (Fig. 4E; supplementary material Table S1).

Interestingly, tgs1 mutant failed to develop resistance against Rif and INH to the extent as the wild type (H37Rv) under multiple-stress, whereas the ability to develop Rif resistance was restored by complementation of the mutant with tgs1 (Table 2).

We thus hypothesized that the bcr1/bcr1 mutant fails to develop a robust biofilm on the oral mucosa at least partly because it is more efficiently cleared by biofilm-infiltrating neutrophils.