ArticlePloS one2013
Elimination of aberrant DRG circuitries in Sema3A mutant mice leads to extensive neuronal deficits.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Semaphorin 3A is a retrograde cell death signal in developing sympathetic neurons.Development (Cambridge, England) · 2016Article
- DRG axon elongation and growth cone collapse rate induced by Sema3A are differently dependent on NGF concentration.Cellular and molecular neurobiology · 2014Article
- R-type calcium channels are crucial for semaphorin 3A-induced DRG axon growth cone collapse.PloS one · 2014Article
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3 authors.
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Abstract
Axon guidance molecules determine the pattern of neuronal circuits. Accuracy of the process is ensured by unknown mechanisms that correct early guidance errors. Since the time frame of error correction in Sema3A null mice partly overlaps with the period of naturally occurring cell death in dorsal root ganglia (DRG) development, we tested the hypothesis that apoptosis of misguided neurons enables error correction. We crossed BAX null mice, in which DRG apoptosis is blocked, with Sema3A null mice to induce errors. Analyses of these double-null mouse embryos showed that the elimination of abnormal projections is not blocked in the absence of BAX. Surprisingly however, there are fewer surviving neurons in Sema3A null or Sema3A/BAX double-null newborn mice than in wild-type mice. These results suggest that guidance errors are corrected by a BAX-independent cell death mechanism. Thus, aberrant axonal guidance may lead to reductions in neuronal numbers to suboptimal levels, perhaps increasing the likelihood of neuropathological consequences later in life.
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