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The conclusion of the paper is highly interesting: that RNA chaperones may buffer mutations that could impact on mRNA folding.
Similar(59)
According to [ 10], a complex network can rapidly achieve the ability to buffer mutations.
In this way, the proper functioning of Hsp90, and other chaperones, may buffer phenotypic expression of mutations even if the chaperones do not physically interact with the mutated proteins.
However, a strong robustness may buffer the accumulation of beneficial mutations.
Chaperones are also highly expressed and may buffer the deleterious effects of the large number of non-synonymous mutations observed in essential T. hominis genes.
Denial may buffer the blow but it cures nothing.
Within forests, however, biodiversity may buffer risk.
The unanswered question is not if RNA chaperones buffer mutations but how.
The finding that protein-coding regions of these genes undergo rapid evolution in humans [ 7- 9] may indicate that the complexity of their network can buffer the mutations in the sequence level more easily.
Similar inferences derive from the capacity of Hsp90 to buffer deleterious mutations in Drosophila development [19].
Following duplication, genes can have many fates: duplicates may amplify or buffer original function [ 29- 31], gain a novel function (neofunctionalization) [ 32, 33], accumulate mutations that subdivide the original function (subfunctionalization) [ 34, 35] or become non-functional (pseudogenization) [ 32].
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