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We show that 18S sequences are more homogenous than ITS1; a pattern that could arise from incomplete rounds of homogenisation and stronger purifying selection acting on the 18S genic region.
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It is acknowledged that incomplete round attendance rate may have had an effect on these results.
We observed myocyte polyploidy in control hearts and increases in myocyte ploidy in the RafAct hearts that is suggestive of incomplete endocycling, repetitive rounds of genome replication.
Therefore, syncytial cysts derived from more than four rounds of incomplete cell divisions are the more parsimonious explanation.
Firstly, germ cells in cysts that have undergone the usual four rounds of incomplete cell division can have at most four ring canals [9], [10] (Fig. 3F).
In region 1, the germline stem cell (GSC) divides to produce a cystoblast, which undergoes four rounds of incomplete cell division to produce a 16-cell interconnected cyst.
A single GSC division gives rise to a cystoblast, which undergoes four rounds of incomplete division to form a 16-cell cyst; the cells of the cyst are interconnected with branched fusomes (Spradling, 1993).
The increased number of ribotypes in ITS1 compared with 18S sequences may reflect rounds of incomplete homogenisation with strong selection for functional genic regions and relaxed selection on ITS1 variants.
In the choanoflagellate Salpingoeca rosetta, rosette-shaped multicellular colonies develop when a single founder cell undergoes multiple rounds of incomplete cytokinesis, leaving neighboring cells physically attached by fine intercellular bridges (Fairclough et al. 2010; Dayel et al. 2011).
The most distinctive effect of these defects is the appearance of double and multi-headed parasites as a result of incomplete daughter abscission and sequential rounds of budding.
Primary spermatogonia then undergo four rounds of mitosis with incomplete cytokinesis, forming cysts of 16 interconnected secondary spermatogonia that then begin meiosis as primary spermatocytes.
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