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Our results have shown that transforming mTOR mutants are distributed across various cancer types (albeit at a low frequency), suggesting that clinical trials with mTOR inhibitors are warranted for individuals with such tumors positive for oncogenic mTOR mutations.

These latter mutants were distributed in an unspecific manner throughout the cytoplasm and were possibly largely cytosolic.

The remaining 28 identified mutants were distributed among 18 mutants (Group 2) (Fig. 3B) which exhibited pinpoint L-form colonies smaller than typical wild type L-form colonies and 10 mutants (Group 3) (Fig. 3C) that displayed a reduction in the number of L-form colonies on LIM.

The relative amount of phospho-Slt2 in these mutants was distributed over a wide range of values (from twice to thirtyfold) (Table 1).

Specifically, the wild-type strain H3T3A and H3K14A mutants were distributed similarly (approximately 13%, 9%, and 11% respectively) while the H3Q5A and H3S57A mutants had increased S-phase populations (approximately 20% and 23% respectively).

The distribution of the deletion mutants (Additional file 9: Figure S7B) indicated that the fitness of most of the 4718 strains was distributed around a central fitness of 1, whereas the heteroclite and the rest of the gene deletion mutants were distributed at a lower fitness level.

After RasV12-induced senescence, HP1γ (wild-type) and HP1γ (S93E) mutant were distributed as large foci and colocalized with H3K9me3, a heterochromatic marker, whereas HP1γ (S93A) mutant was diffusely distributed throughout the nucleus in senescent cells (Fig. 4A).

The wound-induced marker candidates of dde 2 2 mutant plants, for example, are mainly associated with prototypes 10, 12, 16 and 31, while the marker candidates which show accumulation in mutant control plants are distributed among cluster 18 and 32.

Previously described mutant allels of MYO15A are distributed across the length of the gene.

The lesions identified in non-mucoid mutants of S. uberis 0140J are distributed between genetic loci likely to be involved in biosynthesis and also regulation.

Mutant lesions for a given phenotypic class are distributed over large DNA distances of up to 73,000 base pairs.