Nucleotide substitution: G423A. Amino acid replacement: G114D.
G19698359A
G423A
G114D | Cdc42-PA; G114D | Cdc42-PC; G114D | Cdc42-PD
G114D
embryo | anterior | maternal effect (with Cdc426)
embryo | maternal effect (with Cdc426)
nurse cell & actin filament | germ-line clone | maternal effect
Homozygous germline clones result in the arrest of oogenesis and mutant egg chambers develop only until stage 5. From stage 4 onwards, the mutant egg chambers contain 16 polyploid nurse cells instead of the normal 15 nurse cells plus one oocyte. Marker analysis indicates that the oocyte is correctly specified during early stages, but that its fate is not maintained.
Cdc423/+ flies do not exhibit a significantly increased pacing-induced heart failure rate or arrhythmia, do not have significantly different diastolic or systolic intervals, nor any significant disruption in cellular architecture of cardiomyocytes as compared to controls.
Homozygous clones in the wing result in a multiple wing hair phenotype.
Cdc423 mutants have normal embryonic and early larval neuroblast polarity. Third instar larval central brain neuroblasts display polarity defects.
Homozygous Cdc423 mutant embryos do not exhibit a myoblast fusion phenotype.
Hemocytes in embryos dervied from Cdc423/Cdc426 mothers show normal developmental dispersal and normal recruitment to sites of laser-induced tissue damage. However, during the migratory phase and after arrival at the wound site, the mutant hemocytes often possess several leading edges suggesting that they cannot maintain a persistent polarity.
The failure of hemocytes to maintain polarity in embryos dervied from Cdc423/Cdc426 mothers leads the hemocytes to adopt a haphazard migratory route. This defect is countered by the mutant hemocytes migrating at approximately twice the normal speed so that they reach the wound as rapidly as in wild type embryos. On reaching the wound, the mutant hemocytes appear to remain more active than wild type hemocytes, and exhibit exuberant protrusive activity.
Mutant embryos exhibit arrested ganglionic branches (GBs), and GBs turning prematurely away from the midline.
Cdc423/Cdc426 combinations produce over 70% embryonic lethality, even when outcrossed to wild-type males. Embryos produced by Cdc423/Cdc426 mothers display disruptions in epidermal development, including incomplete germband retraction, ventral holes in the epidermis, ventral holes in cuticle produced by epidermal cells, and anterior open phenotypes. Ventral holes range in size from isolated disruptions to openings in the entire ventral surface of the embryo. Patterns of neuronal differentiation are largely normal, even in areas where the integrity of the overlying epidermis is disrupted. In certain embryos defects in the central nervous system, such as incomplete formation and midline fusion of the longitudinal connectives are observed. However, in all embryos the axons of the peripheral nervous system appear to extend properly. Cdc423 somatic clones generated early in larval development do not survive until the wandering third instar larval stage, those generated later (72h AEL) are smaller than sister control clones. No clones survive to adulthood. Even in a Minute background clones in the eye are only visible as scars, not producing any adult ommatidia. Clones in the eye disc do initiate differentiation as photoreceptor cells in the larval eye imaginal disc. In Cdc423 germ-line clones, the cytoplasmic actin filaments that normally form in the nurse cells, although still present are reduced in number compared to wild-type.
Cdc42[+]/Cdc423 is an enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053
Cdc42[+]/Cdc423 is a non-enhancer of abnormal neuroanatomy phenotype of DAAMEx1
Cdc423 is a non-enhancer of abnormal neuroanatomy phenotype of SNF4Aγloe
Cdc42[+]/Cdc423 is a non-enhancer of abnormal neurophysiology | third instar larval stage | recessive phenotype of GluRIIASP16
Cdc423 is a non-enhancer of visible phenotype of Scer\GAL4GMR.PF, pblUAS.cPa
Cdc423 is a suppressor of visible | adult stage phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Cdc42[+]/Cdc423 is a suppressor of abnormal planar polarity phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
Cdc42[+]/Cdc423 is a suppressor of abnormal neuroanatomy phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107
Cdc423 is a suppressor of visible phenotype of Scer\GAL4en-e16E, tumΔE1E.UAS
Cdc423 is a non-suppressor of abnormal neuroanatomy phenotype of SNF4Aγloe
Cdc42[+]/Cdc423 is a non-suppressor of abnormal neurophysiology | recessive | third instar larval stage phenotype of GluRIIASP16
Cdc423 is a non-suppressor of visible phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
Cdc423 is a non-suppressor of visible phenotype of Scer\GAL4GMR.PF, pblUAS.cPa
Cdc42[+]/Cdc423, ExnEY01953/Exn[+], GluRIIASP16 has abnormal neurophysiology | recessive | third instar larval stage phenotype
Cdc42[+]/Cdc423, GluRIIASP16, cacS/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype
Cdc423 has ganglionic tracheal branch primordium phenotype, non-suppressible by RhoGAP93B1
Cdc42[+]/Cdc423 is an enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
Cdc42[+]/Cdc423 is a non-enhancer of adult mushroom body alpha-lobe phenotype of DAAMEx1
Cdc42[+]/Cdc423 is a non-enhancer of adult mushroom body beta-lobe phenotype of DAAMEx1
Cdc42[+]/Cdc423 is a non-enhancer of embryonic/larval neuromuscular junction phenotype of GluRIIASP16
Cdc423 is a non-enhancer of photoreceptor cell | precursor & nucleus phenotype of Scer\GAL4unspecified, msnDN.UAS
Cdc423 is a non-enhancer of larval VL3/4 motor neuron phenotype of PlexBUAS.cHa, Scer\GAL4elav.PLu
Cdc423 is a non-enhancer of larval intersegmental nerve phenotype of PlexBUAS.cHa, Scer\GAL4elav.PLu
Cdc423 is a non-enhancer of eye phenotype of Scer\GAL4GMR.PF, pblUAS.cPa
Cdc423 is a suppressor of eye phenotype of Hsap\TTRV30M.UAS.Tag:HA, Scer\GAL4GMR.PU
Cdc42[+]/Cdc423 is a suppressor of ommatidium phenotype of MtlUAS.cMa, Scer\GAL4hs.2sev
Cdc42[+]/Cdc423 is a suppressor of adult mushroom body phenotype of LIMK1UAS.Tag:HA, Scer\GAL4ey-OK107
Cdc423 is a suppressor of wing vein phenotype of Scer\GAL4en-e16E, tumΔE1E.UAS
Cdc423 is a suppressor of wing phenotype of Scer\GAL4en-e16E, tumΔE1E.UAS
Cdc42[+]/Cdc423 is a non-suppressor of embryonic/larval neuromuscular junction phenotype of GluRIIASP16
Cdc423 is a non-suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
Cdc423 is a non-suppressor of larval VL3/4 motor neuron phenotype of PlexBUAS.cHa, Scer\GAL4elav.PLu
Cdc423 is a non-suppressor of larval intersegmental nerve phenotype of PlexBUAS.cHa, Scer\GAL4elav.PLu
Cdc423 is a non-suppressor of ommatidium phenotype of Rac1V12.hs.sev
Cdc423 is a non-suppressor of eye phenotype of Scer\GAL4GMR.PF, pblUAS.cPa
Cdc423 is a non-suppressor of phenotype of dshhs.sev.B
Cdc423, Pak[+]/Pak6 has adult heart phenotype
Cdc423, Pak[+]/Pak6 has cardial cell phenotype
Cdc42[+]/Cdc423, tin346 has adult heart phenotype
Cdc42[+]/Cdc423, tin346 has cardial cell phenotype
Cdc42[+]/Cdc423, tin346 has cardiac myofibril phenotype
Cdc42[+]/Cdc423, tinEC40 has adult heart phenotype
Cdc423, Df(2L)Exel9032/+ has adult heart phenotype
Cdc423, Df(2L)Exel9032/+ has cardial cell phenotype
Cdc423, Df(3R)BSC397/+ has adult heart phenotype
Cdc423, Df(3R)BSC397/+ has cardial cell phenotype
Cdc42[+]/Cdc423, ExnEY01953/Exn[+], GluRIIASP16 has embryonic/larval neuromuscular junction phenotype
Cdc42[+]/Cdc423, GluRIIASP16, cacS/cac[+] has embryonic/larval neuromuscular junction phenotype
Cdc423/+; Pak6/+ double heterozygotes display severe cardiomyocyte organization abnormalities and contractile abnormalities as compared with either single heterozygote, but no differences in heart beat defects and overall rhythmicity.
Cdc423/+; Df(2L)Exel6012/+ double heterozygotes do not display defects in heart rhythm as compared to controls.
Cdc423/+; Df(2L)Exel9032/+ double heterozygotes and Cdc423/+; Df(3R)BSC397/+ double heterozygotes show significant defects in cardiomyocyte structure, significantly increased arrhythmia, but no significant differences in the overall length of diastolic and systolic intervals.
tin346/+; Cdc423/+ double heterozygotes exhibit a significantly increased pacing-induced heart failure rate, significantly increased arrhythmia and a tendency toward longer diastolic intervals, in addition to severe misalignment of cardiac myofibrils, as compared with controls. These flies do not exhibit differences in systolic intervals.
tinEC40/+; Cdc423/+ double heterozygotes exhibit a significantly increased pacing-induced heart failure rate.
The Cdc423/+ heterozygous mutation does not suppress or enhance the GluRIIASP16 NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc423/+ , GluRIIASP16 double mutants, compared to wild-type or GluRIIASP16 controls.
Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc423/+ and ExnEY01953/+ in a GluRIIASP16 mutant genetic background. There is no deficit in synaptic bouton number in Cdc423/+ , ExnEY01953/+, GluRIIASP16 triple mutants, compared to wild-type or GluRIIASP16 controls.
The combination of Cdc423/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.
Cdc423/+ has very little effect on the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is 10% compared to 9% for control flies expressing LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E in an otherwise wild-type background). The frequency of the malformed leg phenotype seen in Sb63b/+ heterozygotes (8%) is not increased if the flies are also heterozygous for Cdc423/+ (3%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is not increased if the flies are also heterozygous for Cdc423/+ (7%).
Cdc423 is rescued by Cdc42Ubi-p63E.Tag:MYC
Cdc423 is rescued by Cdc42Ubi-p63E.PF