Sentence examples for motility defect in from inspiring English sources
In order to characterize the swimming motility defect in more detail we observed the cells by light microscopy.
They demonstrate that the motility defect in the y241 mutant is due to a transgenic insertion in dual specificity phosphatase 27 (dusp27) that disrupts gene expression.
The ability of the RecA-Htg variant to complement the swarming defect indicates that the lack of RecA is the sole cause of the motility defect in the recA mutant strain.
As previously reported for YFP MglAG21V and YFP MglAQ82L in mglB+ cells (Leonardy et al, 2010; Zhang et al, 2010), YFP MglAR53A and YFP MglAQ82A complemented the motility defect in a Δ mglA mutant (Table I; Figure 8).
The absence of a motility defect in the early larval stages underlines the notion that, in smn-1 ok355 smn-1 ok355otor neurons initianimalstablish normotoruneuronsl connectinitially thestablisht muscles.
Subsequent work by Afzelius [ 5] demonstrated that patients with Kartagener's syndrome had a motility defect in the cilia of respiratory mucosa, in the lungs and sinuses, and that in addition in males there can also be a defect of sperm motility, which results in reduced fertility [ 6].
DOI: http://dx.doi.org/10.7554/eLife.01566.010 One might imagine that the length defect could be the cause of the motility defect if shorter flagella were impaired in their ability to generate a proper flagellar beat, however this does not appear to be the case.
Motility defects in the smn mutant animals are first seen halfway between these stages and are statistically significant by third instar.
Rather the motility defects in Δ mglA and mglAT26/27N mutants are caused by incorrect localization of motility proteins.
Because LIS1 accumulates in flagella when flagellar motility is arrested (Rompolas et al., 2012), the accumulation may be a secondary effect of flagella motility defects in dyf13 mutant.
In this case, it is also possible that the mitochondrial motility defects in higher eukaryotes caused by Miro1/2 dysfunction are a secondary consequence of enhanced ER mitochondria contacts.
