Deletion starting at the Mi{ET1}CG45057MB04349 insertion site in the 5' end of the gene and spanning 3734 base pairs covering 80% of the ringer locus, including the p25α-domain-coding region.
A 3734 bp deletion resulting from the imprecise excision of Mi{ET1}ringerMB04349. The deletion extends from the insertion site into ringer and removes the entire coding sequence. The deletion endpoints were determined from the reported sequence of the junction.
ringer915 mutants show decreased viability at multiple stages of development and less than 40% survive to adulthood. The mutant embryos display misplaced neurons in the ventral nerve cord (while the distribution of midline glia is not affected) and axonal growth and targeting defects (axonal collapse toward midline, mistargeting, stalling, intersegmental axon breaks). Axons from segmental nerves in third instar larvae display disorganized microtubule network and ultrastructural analysis shows defects in microtubule appearance as well as distribution.
ringer915/Df(3L)BSC649 embryos also show neurostructural defects.
ringer915 mutant cultured neurons (primary cultures from larval brains) show axonal extension defects and tend to have much shorter axons than control wild-type neurons.
ringer915 is partially rescued by Scer\GAL4elav-C155/ringerUAS.cMa
ringer915 is partially rescued by Scer\GAL4eve.PU/ringerUAS.cMa
The axonal targeting defects and eve-positive neurons placement errors characteristic for ringer915 homozygous mutant embryos are partially rescued by expression of ringerScer\UAS.cMa under the control of the Scer\GAL4elav-C155 or the Scer\GAL4eve.PU driver, respectively. However, the axonal extension defects observed in cultured ringer915 neurons (primary cultures from larval brains) is not significantly rescued by Scer\GAL4elav-C155-driven expression of ringerScer\UAS.cMa.
