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This entire process is mainly supported by the underlying presynaptic cytoskeleton and induced us to hypothesize that alterations in the organization of these structures might explain the morphological defects observed in TBPH mutant alleles.
Furthermore, we observed that the presence of acetylated MTs in distal presynaptic structures was also rescued by human Tau expression (Figure 5Axiii xv and 5B for quantifications) demonstrating that defects in MT stability were responsible for the morphological defects observed in TBPH mutant boutons.
Furthermore, when grown in the presence of BFA, we found a synthetic enhancement of the morphological defects observed in septin mutants: addition of BFA at permissive temperature (22°C) mimicked the terminal phenotype of septin mutants at high temperature (34°C): round cells that eventually lysed leaving behind cell debris and "ghosts" (Fig. 5B).
The morphological defects observed in Δ ZtCBR1 strains could be representative of an underlying defect in lipid raft formation.
Other than a moderate increase in mortality, there were no consistent morphological defects observed at 24 hpf.
Hence, we concluded that the morphological defects observed in L3 larvae were caused by impairments in dendrite maturation.
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stage before any morphological defect observed.
IUE of HtrA1 in WT cerebral cortices recapitulated morphological and functional defects observed in Gfap Cre Dicer f/f RG cells.
To examine any morphological defects, we observed mature grains under a bright field microscope but did not found any differences between WT and mtd1 1 mutant pollen.
No evidence of outer membrane vesiculation, which has been associated with alterations in σE activity [33], [34], or other gross morphological defects were observed in the TEM or SEM images.
A wide range of morphological defects was observed in the 12 lines.
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