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Sentences for "axonal "
Results ALM migration and PLM axonal morphology defects Figure 2shows fluorescence micrographs and bar graphs of the positions of the ALMs from strain TU2562, which has an integrated mec-3gfp (equivalent to pJC8 in Figure 4), and strain EA485, which contains a high copy extrachromosomal array made from plasmid pJC4 (see Figure 4and Materials and Methods).
Figure 3shows an example of a normal PLM in strain TU2562 and several examples of PLMs with axonal defects in strain EA485.
All of the 189 PLMs scored in TU2562 had normal morphology, whereas 64% of the 183 PLMs scored in EA485 had defects in axonal morphology.
4% of 199 ALMs scored had normal axonal morphology, whereas in TU2562, all of the 117 ALMs scored had normal morphology.
The majority of ALMs with abnormal axonal morphology were in positions 1-3 with a few as posterior as position 5.
All ALMs located posterior to position 5 had normal axonal morphology.
The migration defect was not due to nonspecific effects of carrying an array, expression of GFP, or the rol-6 transformation marker gene The above data also show that the ALM migration and PLM axonal morphology defects are not due to nonspecific effects of carrying an extrachromosomal array.
17 and pJC1 had little effect on ALM migration and PLM axonal morphology.
The above results, however, show that neither the migration defects nor the PLM axonal morphology defects resulted from expression of GFP.
17 and pJC1, express GFP yet had few ALM migration or PLM axonal morphology defects.
Because some of these arrays, and others described below, did not induce ALM migration or PLM axonal defects, these phenotypes were not due to the rol-6 marker plasmid.
In the case described here, it seemed unlikely that RNAi was inducing the ALM migration or the PLM axonal morphology defects because there is no predicted protein-encoding gene in the titrating sequence.
These RNA injected animals also had normal PLM axonal morphology.
Therefore, the ALM migration and the PLM axonal morphology defects were not due to RNAi.
The ALM migration and the PLM axonal morphology defects are highly correlated Strains that had many ALM migration defects also had many PLM axonal defects.
58 more results not shown.
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