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Based on a Homarus americanus (lobster) outgroup, these were generated through gene duplication events on major beta and alpha tubulin ancestors, followed by subfunctionalization in expression domain.
Yet gene duplication is not sufficient to release tubulin evolution, most duplication products are lost, and major tubulin duplication products do not evolve unless followed by subfunctionalization in expression domain.
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Gene duplication, subfunctionalization in expression domain, and divergence, particularly in CTT sequences has resulted in the specialized, minor tissue-specific insect isoforms.
Taken together, these observations suggest that subfunctionalization in expression has taken place after the divergence of Gal-1A and Gal-1B.
They evolve through gene duplication, subfunctionalization in expression domain and divergence of duplication products, largely in CTT residues that mediate interactions with other proteins.
The members persisted after initial duplications by undergoing subfunctionalizations in their expression patterns and target site recognition.
The duplication of this progenitor was followed by subfunctionalization of gene expression to give rise to tissue-specific c-Myb and A-Myb genes.
The duplication of this progenitor was followed by subfunctionalization of gene expression to give rise to tissue-specific c- Myb and A- Myb genes.
Neofunctionalization and subfunctionalization in the expression of the different paralogs is due to differences in promoter structure/function as the genes are differentially expressed by these different myogenic conditions.
Gene duplication followed by subfunctionalization resulted in proneural ASH and precursor-specific ase-like genes independently in Tetraconata and chelicerates.
From this observation, it appears unlikely that all temporal subfunctionalization will be caused by regulatory subfunctionalization in normal conditions.
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