Amino acid replacement: A126T.
Point mutation within the active site of the kinase which is involved in phosphorylation.
G17870363A
A191T | mnb-PE; A191T | mnb-PF; A191T | mnb-PG; A330T | mnb-PH; A330T | mnb-PI
A126T
Position of mutation on reference sequence inferred by FlyBase curator based on author statement.
NMJ bouton (with Df(1)RR79)
mnb1/mnb1 mutants exhibit a significant increase in proliferation of ganglion cells, but not neuroblasts or ganglion mother cells; and show a significant increase in the number of apoptotic cells in the outer proliferation center and central brain of late third instar larvae, as compared to wild type.
mnb1 mutant NMJs have fewer synaptic boutons than controls, but the remaining boutons are larger in size.
mnb1/Df(1)RR79 mutant NMJs have fewer synaptic boutons than controls, but the remaining boutons are larger in size.
mnb1 mutants have increased miniature excitatory postsynaptic potential (mEPSP) amplitude but normal evoked EPSP amplitudes. When the nerve is stimulated at a high frequency (10Hz) for a prolonged period (10 minutes), mnb1 shows a significantly faster rundown than controls.
mnb1 mutant larvae exhibit synaptic vesicle endocytosis defects: the level of membrane uptake (dye internalisation) in mutant synaptic boutons in response to nerve stimulation is significantly reduced compared to controls. When dye unloading occurs in response to a second stimulation, the mnb1 mutants unload a similar amount of dye to controls, suggesting exocytosis is unaffected.
mnb1/Df(1)RR79 mutant larvae exhibit synaptic vesicle endocytosis defects: the level of membrane uptake (dye internalisation) in mutant synaptic boutons in response to nerve stimulation is significantly reduced compared to controls. When dye unloading occurs in response to a second stimulation, the mnb1/Df(1)RR79 mutants unload a similar amount of dye to controls, suggesting exocytosis is unaffected.
Reduced brain volume, neuronal architecture has no gross alterations. External appearance is wild type, body size is slightly smaller than wild type. Mutants require 10% more time for their development and have considerable difficulty escaping from the pupal case. Adults exhibit defects in olfactory and visual behaviour. The neuroblast proliferation centre in larval brains is altered, unable to generate sufficient numbers of optic lobe and central brain neurons.
Reduction in fibre number in the anterior optic tracts.
mnb1 has abnormal neuroanatomy phenotype, suppressible | partially by SynjUAS.Tag:HA/Scer\GAL4nSyb.PS
mnb1 has abnormal neurophysiology phenotype, suppressible by SynjUAS.Tag:HA/Scer\GAL4nSyb.PS
mnb1 has abnormal neuroanatomy phenotype, suppressible | partially by Scer\GAL4nSyb.PS/Avic\GFPEGFP.UAS.Tag:PH(hPLCD1)
mnb1, rol1, sol1 has abnormal neurophysiology phenotype
mnb1 has NMJ bouton phenotype, suppressible | partially by SynjUAS.Tag:HA/Scer\GAL4nSyb.PS
mnb1 has NMJ bouton phenotype, suppressible | partially by Scer\GAL4nSyb.PS/Avic\GFPEGFP.UAS.Tag:PH(hPLCD1)
Expression of SynjScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4nSyb.PS suppresses the increase in bouton size in mnb1 mutant NMJs, but does not suppress the reduction in bouton number.
Expression of SynjScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4nSyb.PS significantly rescues the excitatory postsynaptic potential (EPSP) amplitude defects seen in response to high frequency stimulation seen in mnb1 mutant larvae. However these larvae also show a slightly faster rundown than controls after prolonged stimulation. The miniature EPSP (mEPSP) and endocytosis defects are also rescued.
Expression of Hsap\PLCD1PH.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4nSyb.PS suppresses the increase in bouton size in mnb1 mutant NMJs, but does not suppress the reduction in bouton number.
mnb1 is rescued by mnbUAS.Tag:HA/Scer\GAL4nSyb.PS
Pre-synaptic expression of mnbScer\UAS.T:Ivir\HA1 under the control of Scer\GAL4nSyb.PS rescues the bouton and miniature excitatory postsynaptic potential (mEPSP) defects seen in mnb1 mutants. The synaptic vesicle endocytosis defects are also rescued.
Heisenberg.