One third of the guanylate kinase domain is deleted.
14bp deletion starting at 2528bp that shifts the reading frame and deletes two thirds of the GUK domain.
Eliminates most of the guanylate kinase domain.
14bp deletion in guanylate kinase domain: introduces a stop codon after 12 amino acids.
14bp deletion in guanylate kinase domain; introduces a stop codon after 12 amino acids.
Follicle cells do not have an invasive phenotype in females with homozygous dlg16 clones in the germ cells and follicle cells.
Presynaptic morphology is normal. Structural defects in the subsynaptic reticulum (SSR), it appears to be underdeveloped. Synaptic transmission is altered; increase in excitatory junctional currents (EJC) amplitude (not due to changes in passive properties of the muscle membrane but due to presynaptic defects causing increased neurotransmitter release).
The subsynaptic reticulum (SSR) expands more slowly than wild-type and never reaches the final length of wild-type SSR in hemizygous flies. There are no abnormalities in the pathways axons follow, the growth cone morphology, or the time at which the growth cones reach their target and differentiate into boutons on muscles 6, 7, 12 and 13 in hemizygotes.
Homozygous larval show overgrowth of the imaginal discs. Salivary gland cells show no obvious morphological or ultrastructural defects.
Lethality occurs during metamorphosis with neoplastic growth in imaginal discs and CNS. The morphology of the synaptic bouton structure is altered and the subsynaptic reticulum (SSR) is substantially less extensive and less complex than in wild type.
Geer.
Class III mutation.