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Prior to glaciations, an integrated karstic aquifer could develop with flow controlled by conduits; however, this original, converging flow system became non-functional when the Quaternary sediments drastically modified the boundary hydrologic conditions and the head distribution.
Lift nets were minimally damaged, but irrespective of the deployment duration, all hoop nets had broken/missing meshes (lost as marine debris), and those left for up to 12 days quickly became non-functional.
Our analysis of the GC-D gene shows that it became non-functional early in primate evolution; this event occurred either prior to the divergence of tarsiers, New World monkeys and catarrhine primates, or independently early in each lineage.
Alternatively, there may have been insufficient time for the genes to become highly diverged since they became non-functional.
The latter became non-functional, subject in the course of evolution to gradual elimination from the genome accompanying the loss of function.
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A central model that has been strongly supported by Ohno [ 56] states that a duplicate gene can accumulate mutations and become non-functional (non-functionalization) or diverge to a novel function (neo-functionalization) while the other duplicate keeps its original function.
Many duplicated genes have a short lifespan, as one of the two copies is either lost or degenerates and becomes non-functional (non-functionalization).
Indeed, following a duplication, the most common occurrence is for only one of the two gene copies to maintain the parental function, while the other becomes non-functional (pseudogenization) or acquires a new function (neofunctionalization) [ 3].
Gene duplication events are purported to lead to three successful functional outcomes: i) one of the duplicated genes can preserve the same function as before duplication (sub-functionalization), ii) one of the duplicated genes can acquire a new function (neo-functionalization), or iii) one of the duplicates can become non-functional [ 1, 90].
In turn, photosynthesis is modeled as a function of the number of functional photosystem II (PSII) subunits, which become non-functional when their D1 core proteins are damaged, and regain their function when the damaged D1 is excised from the photosystem and replaced with the protein product of either a host or phage psbA gene (Fig. 1).
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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