The phrase "alignment defect" is correct and usable in written English.
It can be used in contexts related to engineering, manufacturing, or any field where alignment is critical, indicating a flaw or issue in alignment.
Example: "The technician identified an alignment defect in the machinery that needed immediate attention to prevent further issues."
Alternatives: "misalignment issue" or "alignment error".
We confirmed the microtubule alignment defect caused by oMAP4 depletion results by tracking growing microtubule ends labelled with EB3-tdTomato.
In addition, we find that the alignment defect of GAK-depleted cells can only be reverted by variants of GAK that are able to recycle clathrin from endosomes.
RNAi-resistant GFP-CENP-Mwt localized to kinetochores and rescued the severe chromosome alignment defect caused by the depletion of endogenous CENP-M by RNAi, as well as kinetochore localization of CENP-I, demonstrating the specificity of the RNAi-based depletion of CENP-M.
The early defect in OFT elongation is likely to underlie the subsequent ventriculoarterial alignment defects observed in fetal Hes1−/− hearts.
Remaining prometaphases displayed alignment defects, indicative of a rescue from the lack of KT-MT interaction (Figure 2B, graph).
Analysis of Hes1 mutant hearts at embryonic day 15.5 reveals outflow tract alignment defects including ventricular septal defects and overriding aorta.
aPKCAA did not cause any apparent apical-basal phenotype, but in contrast to aPKCΔN (Fig. 6C), aPKCAA did cause denticle alignment defects (Fig. 6D).
Previous studies have reported that GSK3 inhibition results in a delay in mitotic exit, and this phenotype has been largely attributed to chromosomal alignment defects [3], [5].
Loss of Hes1 therefore affects two critical cell populations entering the arterial pole of the heart, the SHF and cardiac neural crest cells, leading to impaired heart tube elongation and arterial pole alignment defects at later stages of development.
OFT alignment defects in Hes1 mutant embryos have been independently observed by another group who, in addition, noted aortic arch artery abnormalities associated with a defective smooth muscle contribution at E11.5 (P. Scambler, personal communication).
Indeed, no overt mitotic phenotypes were observed except for an induction of chromosome alignment defects, i.e. late prometaphase cells in which few KTs localized external to the metaphase plate (Figure 1D, second row).
