The increase observed in longevity associated with the ATPalpha CJ6, ATPalpha CJ12 and in ATPalpha DTS1R1 mutations was reproduced (Fig. 7b).
The high mutation frequencies of the dms4-1 suppressor mutations were reproduced in a second trial of EMS mutagenesis using a more advanced generation of dms4-1 seeds (BC2F4).
However, it is encouraging that rare mutations were reproduced in independent studies, including GATA3 mutations in estrogen receptor-positive disease [ 2- 4], ERBB2 mutations in TNBC [ 1, 3], and TBX3 [ 2, 4], CBFB, and/or RUNX1 mutations [ 2, 3].
The effects of these mutations were reproduced in the RNA splicing process using both an overexpression model and patient samples, but were not seen in cell growth of experimental models such as repopulation assays.
This finding was reproduced in a mouse strain carrying another spontaneous mutation in Ncf1 and with nearly absent ROS production [ 56, 80].
This imagery was reproduced in the series.
Critically, the phenotypes associated with the pilX and pilV mutations could be reproduced by matching the mean number of pili associated with those knock-out strains.
Interpretations of certain mutations could not be reproduced in some instances.
Like an organism, an organ such as the bacterial flagellum requires particular genes to be reproduced, and mutations in these genes are physical marks of possible transformations of this organ.
Importantly, the sensitivity of 3/4 of these cells bearing mutations in TP53 couldn't be reproduced (P12-ICHIKAWA, KBMC-2 and Hs 294T with IC50 > 8 µM), while the sensitivity of the NCI-H2122 TP53 mutant cell line was confirmed in repeat cell proliferation assays.
