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Future studies focusing on the relationship between the morphological defects and neuronal function will have to shed light on this issue.
These experiments provide evidence that the lethality observed in the miR-6 miR-11 double mutants was caused by elevated proapoptotic gene expression, and show a correlation between the morphological defects in the CNS and lethality.
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As not all hemisegments in homozygous mutant embryos exhibit this latter phenotype, we assessed whether there is any correlation between the de-repression of a specific gene and the morphological defects associated with mutations in jumu or CHES-1-like.
Extensive apoptosis was observed in the head region of the morphants, thus correlating the morphological defects with apparent cell death.
The morphological defects observed in Δ ZtCBR1 strains could be representative of an underlying defect in lipid raft formation.
However, the morphological defects became less evident when cultured on cellulose medium.
Many diagnostic indices do not properly reflect the morphological defects, and there is little international standardisation.
Defects in membrane potential, respiratory distress and inefficient transport can all secondarily contribute to the morphological defects associated with mutant Htt expression.
Furthermore, the morphological defects of stereocilia in Pls1 KO are consistent with an abnormal maintenance of their actin content.
Many diagnostic indices however, do not properly reflect the morphological defects and furthermore there is little international standardisation.
Hence, we concluded that the morphological defects observed in L3 larvae were caused by impairments in dendrite maturation.
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