One partially deleted insertion in the first intron and the second partially deleted insertion resides in the original location.
14-3-3ζ12BL heterozygous larvae do not have reduced amplitude of evoked excitatory junction potentials in the neuromuscular junction, compared to controls.
Homozygous follicle cell clones are recovered only at a low frequency, compared with sibling wild-type clones. Those mutant follicle cell clones that do survive have severe morphological defects.
Homozygous embryos exhibit incomplete dorsal migration of the lateral epidermis and failure of dorsal epidermal closure. CNS and neuromusculature appear morphologically normal and the mutant embryos exhibit coordinated muscle movements similar to those observed in wild-type locomotion. Synaptogenesis at the neuromuscular junction (NMJ) is largely normal. Embryos also exhibit near normal physiological development and basal excitation-secretion function at the NMJ. The amplitude and frequency of endogenous excitatory junctional currents (EJCs) is reduced relative to wild type. This reduced function originates in a presynaptic defect, basal presynaptic function is mildly impaired. MEJC (miniature EJCs) amplitude is not altered. NMJ exhibits a transmission defect, the calcium dependence curve is shifted to the right indicating a higher level of external calcium is required to achieve the given level of secretion. Synaptic transmission fidelity and fatigue resistance properties are impaired. Short-term facilitation is strengthened but synaptic augmentation an potentiation are disrupted.
14-3-3ζ12BL/14-3-3zeta[+] is an enhancer of visible phenotype of Scer\GAL4GMR.PF, ykiUAS.Tag:MYC
14-3-3ζ12BL, cindr1/cindr[+] has abnormal neurophysiology | larval stage phenotype
14-3-3ζ12BL/14-3-3zeta[+] is an enhancer of eye phenotype of Scer\GAL4GMR.PF, ykiUAS.Tag:MYC
14-3-3ζ12BL, cindr1/cindr[+] has embryonic/larval neuromuscular junction phenotype
cindr1/+, 14-3-3ζ12BL/+ double heterozygous larvae have significantly reduced amplitude of evoked excitatory junction potentials in the neuromuscular junction, compared to controls.
14-3-3ζ12BL/+ rescues the increased vacuolation of hemo-A4/hemo-A4 mutant hemocytes.
The eye overgrowth phenotype caused by expression of ykiScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF is enhanced by 14-3-3ζ12BL/+.