Imprecise excision of the P{EP} element removing the entire coding region and extending 1867bp downstream of the transcription unit.
embryonic neuroblast & spindle | germ-line clone
Mesoderm invagination is delayed (mesoderm breadth is significantly reduced) and posterior midgut is variably affected (the anterior movement of pole cells due to posterior midgut invagination and tissue extension is defective) in Gβ13FΔ1-96A/Gβ13FΔ1-96A embryos (germline clones) compared to controls.
Gβ13FΔ1-96A/+ larval neuromuscular junctions show no significant change in bouton number in comparison to wild-type neuromuscular junctions.
Embryos derived from homozygous female germline clones show morphological defects during gastrulation which lead to the formation of anterior and posterior holes in the cuticle. Neuroblasts delaminate normally and enter mitosis shortly after delamination in these embryos. Only 26% of the asymmetric cell divisions in the mutant neuroblasts are oriented along the apical-basal axis (as occurs in wild type), other divisions are misoriented by more than 30 degrees.
Gbeta13F[+]/Gβ13FΔ1-96A, mGluR112b has bouton phenotype
A Gβ13F/+ background suppresses the increase in synaptic bouton number seen when mGluRAScer\UAS.cRa is expressed under the control of Scer\GAL4OK6 in a wild-type background.
mGluRA112b/+; Gβ13FΔ1-96A/+ double mutant larvae show an increase in synaptic bouton size that is not seen in either single mutant heterozygote. The bouton number is not changed in the double mutants.
Gβ13FΔ1-96A is rescued by Gβ13F+tSa