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As shown above, WalKR-depleted cells exhibit abnormal division septa and a rougher cell surface.
The grp23 showed abnormal division in both apical and basal cell development.
We propose that a tight phenotypic linkage between the cause of cytokinesis failure and stimulated cell growth and proliferation offsets the intrinsic cost of abnormal division and polyploidy on cell survival.
We have shown here that WalKR depletion leads to a rougher cell surface, abnormal division septa and a defect in cell separation, but that cell viability is restored when LytM or SsaA are overproduced.
At low drug concentrations that permitted cell division, spindle position was highly displaced from normal, resulting in abnormal division planes.
MCD appears as at least two major phenotypes: One is mitosis associated cell death, which occurs following abnormal segregation, where death takes place in G1 following abnormal division.
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The monopteros mutant, for example, is expressed in the Arabidopsis embryo, and the mutant is characterized by abnormal divisions in the prospective procambial tissue in the embryo and defective cotyledonary vein formation [10], [11].
The preponderance of multipolar spindles likely resulted in many of the abnormal divisions.
Cytokinesis bisects the spindle in fucoid zygotes [ 27], so it was not surprising to find abnormal divisions following monastrol treatment.
BTRC loss of function in mice results in slow progression through meiosis and abnormal divisions in spermatocytes [ 19].
Taken together, these results suggest that CYCD1 1 and CYCD3 3 drive the abnormal divisions in the wox5-1 QC.
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