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Intra-specific genetic variation in disease susceptibility to Perkinsus marinus was indirectly demonstrated by the evolution of resistance in disease-challenged natural populations of oysters [ 13].
As demonstrated by the evolution of mitochondria and chloroplasts, endosymbiosis is a major driving force behind eukaryotic cell evolution leading to acquisition of new intracellular components and cell diversity [ 1, 2].
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Genetic variation plays a major role in adaptive evolution, as demonstrated by the rapid evolution of highly expressed genes in the brains of dogs linked to the evolution of dog-specific characteristics [ 83].
The feasibility of this approach is demonstrated by the new evolution of our monitoring system prototype, SIMBAD, where the first biomedical signal processing applications are implemented.
The startup is best demonstrated by observing the evolution of the various parameters on an oscilloscope during the sequence.
Lastly, the evolution of a hydrogenosomal polyprotein requires only the acquisition of a single mitochondrial targeting signal, which can be acquired easily as demonstrated by the frequent retargeting of proteins in the evolution of the eukaryotic cell [ 31, 32].
The presence of an association with liver pathology will only lead to worsening the evolution, as was demonstrated by the data in the literature.
The interaction of frataxin in complex with both the Fe-S scaffold and the cysteine desulfurase is most likely conserved throughout evolution, as demonstrated by the co-purification of Isu/Nfs1 with Yfh1 in yeast [11] and IscU/IscS with CyaY in bacteria [12].
This autosome-specific binding is conserved in evolution, as demonstrated by the F element specificity (also detected, for instance, in Drosophila pseudoobscura and Drosophila virilis).
Furthermore, some genes could change functions in course of the vertebrate evolution as demonstrated by the identification several genes known as neural specific in mammals were primarily involved in innate antiviral responses in fish [ 77, 78].
We propose that the abundance of horizontal gene transfers in free-living prokaryotes is a simple but necessary consequence of two opposite effects: i) their apparent genome size constraint compared to typical eukaryote genomes and ii) their underlying genome expansion dynamics through gene duplication-divergence evolution, as demonstrated by the presence of many tandem and block repeated genes.
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