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We suspect, however, that migration defects are particularly important.
Fz3 −/− embryos also exhibit subtle defects in the migration of monoaminergic neurons (Fenstermaker et al., 2010) and more severe defects in the migration of VIIth cranial nerve neurons (Qu et al., 2010), but, in general, neuronal migration defects are not a prominent feature of the Fz3 −/− phenotype.
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Tracheal migration defects were milder in h674mutant embryos although delayed migration of DT cells was apparent (Figure 2F and I).
Migration defects were also observed with this approach.
These cell migration defects were potentially caused by defects in cell adhesion mechanisms.
DTC migration defects were scored in adult animals using differential interference contrast microscopy.
How misregulation of string might contribute to the migration defects is less immediately obvious.
DTC migration defects were inferred from the resulting shape of the gonad arms.
BANCR was identified as a potential regulator of melanoma cell migration as profound migration defects were observed following BANCR depletion.
Migration defects were observed, comparable with those induced by α5 integrin silencing, with an accumulation of migrating neurons in the ventral region of the cortex (Fig. 4A).
RNAi lines that resulted in more than 9% of egg chambers with border cell migration defects were classified as positive hits.
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