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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 

Pathology of the adult central nervous system induced by genetic inhibition of programmed cell death in Drosophila pupae.

In the spinster (spin) mutant of Drosophila melanogaster, the extent of programmed cell death (PCD) in the abdominal ganglion 6 h after puparium formation (APF) is significantly reduced. The shortening of the abdominal ganglion, which is normally completed 48 h APF, does not occur. After eclosion, neurodegeneration accompanied by accumulation of autofluorescent materials is manifested in the central nervous system (CNS) of the spin mutant. The materials accumulated in the spin-mutant CNS contain a substance that is immunopositive to an antibody against GM2 ganglioside. Halving the dosage of three cell death genes, rpr, grim, and hid, blocks shortening of the abdominal ganglion and induces neurodegeneration accompanied by accumulation of autofluorescent materials in the adult CNS. These observations suggest that the primary action of the spin mutation is to reduce the extent of PCD 6 h APF, which concomitantly leads to a failure in shortening of the abdominal ganglion and to neurodegeneration of the adult CNS. Arch.[1]

References

  1. Pathology of the adult central nervous system induced by genetic inhibition of programmed cell death in Drosophila pupae. Usui-Aoki, K., Nakano, Y., Yamamoto, D. Arch. Insect Biochem. Physiol. (2002)
 
 
 
 
 
 
 
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