Likewise, the psi mutation shows less sensitivity to auxin than the wild type, and enhances the ability to maintain the auxin response in the root tip under low P supply (X.M. Wang et al., 2010).
In contrast to the clustered mutations, which had the same mutational APOBEC signature as the top strand lesions, the unclustered mutations show less of a preference towards mutating the C of TpC, most evident for those induced by restoration of T/G to C/G (cf. lower 2 panels, Figure 5A and the lower panels labeled unclustered, Figure 5B).
The formation of conspicuous and well-demarcated amyloid plaques is typically seen in inherited forms with codon P102L (Figs. 4m, 5c) P105L, and A117V mutations (Figs. 4n, 5d), whilst D178N or E200K (Figs. 4o, 5e) mutations show less well-defined plaque pathology.
The portion of the AChE2 gene after the recombination breakpoint, which is linked to the resistance-associated mutation S291G, showed less allelic variability than the portion before the recombination breakpoint (see Figures 2A and B).
As shown previously, [ 33] Ig-VH3 gene rearrangements of DN B cells Ig-R showed less mutation compared to pre-switch and post-switch B cells.
We have found that two Abs with broad and potent ADCC activity originated from unique B cells and showed less mutation from germline than bnAbs.
Consistent with this theory, it was found in several different systems that frameshifting efficiency was generally more sensitive to mutations introduced to S1 & L2, and the junction, while mutations to S2 & L1 showed less effect on frameshifting efficiency, as long as integrity and stability of the pseudoknot-forming interaction were maintained [ 25, 63– 63].
One MDD subject carried essentially a homoplasmic mutation in DLPFC at ND4L T10652C, and two subjects with SZ showed less than 1% heteroplasmy; however, the pathological significance of the low levels of this non synonymous heteroplasmic mutation is unknown.
Further, they showed less phenotypic overlap with patients who had de novo truncating mutations in ASXL1.
Mutations at codon 600 showed several hundred fold elevation of kinase activity while others showed less than 100 fold elevation.
