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Population genetics characterizes the mutational decay in time of the adaptation module in the population.
To search for natural mutational decay in C. briggsae, we analyzed nearly complete mitochondrial genome sequences (13,430/14,420 total bp) from 24 geographically diverse C. briggsae natural isolates (Table 1).
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If L1 elements are indeed major players in this process, then loss of L1 activity in a species, followed by the mutational decay seen in previously deposited L1 sequences as they mutate over time, should have repercussions for X inactivation.
Our prediction of a genomic decay paradox strengthens the conclusions of earlier work that suggested the existence of additional biological processes that slow down or halt the mutational decay of fitness in this fish.
Such differences in mutational decay have previously been identified in C. elegans and among several other nematode species [30].
It is also possible that there has not yet been sufficient mutational decay of previously deposited L1s in O. palustris to elicit obvious compensatory evolution from homologous Xist sequences or that the new G repeat is the result of compensatory evolution in the presence of deteriorating L1 elements.
Thus, differences in insertion deletion mutation processes, rather than base-substitution events, are potentially responsible for the observed variation in the mutational decay of fitness between these two species.
Many of these prophages are cryptic and in a state of mutational decay.
Prophages can also be defective (in a state of mutational decay and not induced to lytic growth) or be satellites (not carrying their own structural protein genes but capable of encapsidation by capsid proteins of other virions) [5].
Pseudogenes undergo mutational decay and would eventually become unrecognizable, but in practice ambiguous cases were not encountered.
The rapid fitness loss was hypothesized to be due to mutational decay caused by chromosomal copy number changes in the macronucleus.
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