Phenotypes:

Alleles for which the sequence change is known are listed in boldface.

The following phenotypes have been observed in unc-77:

Phenotype Entities Affected Supporting Evidence
nose movement variantAllele:
head bend angle variantAllele:
exaggerated body bendsAllele:
e625
Curator: Karen Yook
Ease of scoring: Es2 difficult to score
Person evidence: Jonathan Hodgkin
Remark: irregular loopy movement both forward and reverse; slight movement abnormality in e625/+
Semi dominant: Person_evidence; Curator_confirmed
details
forward point velocity decreasedAllele:
coilerAllele:
hp102
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Mutants showed semi-dominant, uncoordinated, and exaggerated body bends during either spontaneous or stimulated locomotion.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
shortAllele:
shortAllele:
thinAllele:
tail bend angle decreasedAllele:
coiling frequency increasedAllele:
endogenous synaptic event frequency reducedAllele:
e625
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Some animals displayed a normal frequency of mPSC while others had no mPSC at all.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
body posture wavelength decreasedAllele:
protruding vulvaAllele:
e625
Curator: Karen Yook
Person evidence: Jonathan Hodgkin
Remark: sometimes protrusive vulva
details
roaming reducedAllele:
forward locomotion variantAllele:
evoked postsynaptic current variantAllele:
hp102
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: No ePSC could be evoked.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
amplitude of sinusoidal movement variantAllele:
constitutive egg layingAllele:
synapse morphology variantAllele:
hp102
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Animals exhibited unusually large HSN synapses.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
pausing decreasedAllele:
backward point velocity decreasedAllele:
body posture amplitude decreasedAllele:
backing decreasedAllele:
body posture amplitude increasedAllele:
endogenous synaptic event frequency reducedAllele:
hp102
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Some animals displayed a normal frequency of mPSC while others had no mPSC at all.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
thinAllele:
locomotion variantAllele:
e625
Curator: Carol Bastiani
Paper evidence: Brenner S, 1974
details
synapse morphology variantAllele:
e625
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Animals exhibited unusually large HSN synapses.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
constitutive egg layingAllele:
path curvature variantAllele:
pausing variantAllele:
transgene subcellular localization variantAllele:
hp102
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Animals exhibited abnormal active zone marker distribution.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
body posture wavelength decreasedAllele:
path curvature increasedAllele:
backward point velocity variantAllele:
frequency of body bend variantAllele:
forward point velocity variantAllele:
turning frequency variantAllele:
tail bend angle variantAllele:
forward locomotion decreasedAllele:
amplitude of sinusoidal movement increasedAllele:
frequency of body bend variantAllele:
coiling frequency decreasedAllele:
head bend angle variantAllele:
turning frequency increasedAllele:
coilerAllele:
e625
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Mutants showed semi-dominant, uncoordinated, and exaggerated body bends during either spontaneous or stimulated locomotion.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
nose movement decreasedAllele:
evoked postsynaptic current variantAllele:
e625
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: No ePSC could be evoked.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
backward locomotion variantAllele:
transgene subcellular localization variantAllele:
e625
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: Animals exhibited abnormal active zone marker distribution.
Semi dominant: Curator_confirmed; Paper_evidence
Variation effect: Hypermorph gain of function; Curator_confirmed; Paper_evidence
details
protein degradation variantRNAi:
WBRNAi00090483
Genotype: ccIs55 [unc-54::lacZ]; daf-18(e1375)
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
Remark: The daf-18(e1375) mutation failed to suppress the RNAi-induced increase in muscle protein degradation, as determined by LacZ staining, suggesting that this increase in degradation is not dependent on the daf-18 gene or the Insulin-like signaling pathway, of which daf-18 is a part.
details
protein degradation variantRNAi:
WBRNAi00090389
Genotype: ccIs55 [unc-54::lacZ]; unc-51(e369)
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
Remark: The unc-51(e369) mutation failed to suppress the RNAi-induced increased in muscle protein degradation, as determined by LacZ staining, suggesting that this increase in degradation is not dependent on the unc-51 gene or the Autophagy pathway, of which unc-51 is a part.
details
protein degradation variantRNAi:
WBRNAi00090436
Genotype: ccIs55 [unc-54::lacZ]; mpk-1(n2521)
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
Remark: The mpk-1(n2521) mutation failed to suppress the RNAi-induced increased in muscle protein degradation, as determined by LacZ staining, suggesting that this increase in degradation is not dependent on the mpk-1 gene or the Fibroblast Growth Factor pathway, of which mpk-1 is a part.
details
protein degradation variantRNAi:
WBRNAi00089961
Genotype: ccIs55 [unc-54::lacZ]
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
Remark: RNAi was observed to significantly reduce cytosolic protein levels in body wall muscles, as determined by reduced LacZ staining compared to controls. This affect was observed after chronic RNAi exposure (RNAi continuously for two generations), as well as after acute exposure to RNAi only during adulthood.
details
protein degradation variantRNAi:
WBRNAi00090530
Affected by molecule: MG132
Genotype: ccIs55 [unc-54::lacZ]
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
Remark: The proteasome inhibitor MG132 failed to suppress the RNAi-induced increase in muscle protein degradation, as determined by LacZ staining, suggesting that this increase in degradation is not dependent on the proteasome.
details
mitochondria morphology variantanatomy-term: body wall muscle cell, abnormalRNAi:
WBRNAi00090279
Genotype: ccIs4251 [Pmyo-3::MitGFP, Pmyo-3::NLS::GFP-lacZ]
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
Remark: RNAi was observed to significantly perturb mitochondrial morphology in body wall muscles, as determined by observation of a muscle-specific fluorescent mitochondrial reporter. This affect was observed after chronic RNAi exposure (RNAi continuously for two generations), as well as after acute exposure to RNAi only during adulthood.
details

Phenotype not observed:
The following phenotypes have been reported as NOT observed in unc-77
Phenotype Entities Affected Supporting Evidence
activity level variantAllele:
e625
Curator: Karen Yook
Person evidence: Jonathan Hodgkin
Remark: active
details
locomotion variantAllele:
gk9
Curator: Karen Yook
Paper evidence: Yeh E et al., 2008
Remark: The single mutant displays normal locomotion.
Variation effect: Loss of function undetermined extent; Curator_confirmed; Paper_evidence
details
lethalAllele:
tm1851
Curator: Karen Yook
Person evidence: National Bioresource Project c/o Dr. Shohei Mitani
Remark: Classified as homozygous viable by the National Bioresource Project of Japan.
details
organism morphology variantRNAi:
WBRNAi00040345
Paper evidence: Sonnichsen B et al., 2005
details
sterile progenyRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
body wall muscle sarcomere morphology variantanatomy-term: body wall muscle cell, abnormalRNAi:
WBRNAi00090121
Genotype: jIs01 [myo-3::GFP], translational fusion
Paper evidence: Shephard F, Adenle AA, Jacobson LA & Szewczyk NJ, 2011
details
maternal sterileRNAi:
larval arrestRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
larval lethalRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
slow growthRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
dumpyRNAi:
lethalRNAi:
nematode phenotypeRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
nematode phenotypeRNAi:
WBRNAi00028805
Paper evidence: Rual JF et al., 2004
details
maternal sterileRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
nematode phenotypeRNAi:
exploded through vulvaRNAi:
sterile progenyRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
embryonic lethalRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
organism morphology variantRNAi:
embryonic lethalRNAi:
growth rate variantRNAi:
larval arrestRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
embryonic lethalRNAi:
WBRNAi00040345
Paper evidence: Sonnichsen B et al., 2005
details
rollerRNAi:
lethalRNAi:
WBRNAi00028805
Paper evidence: Rual JF et al., 2004
details
organism morphology variantRNAi:
WBRNAi00040346
Paper evidence: Sonnichsen B et al., 2005
details
organism morphology variantRNAi:
nematode phenotypeRNAi:
WBRNAi00040346
Paper evidence: Sonnichsen B et al., 2005
details
maternal sterileRNAi:
larval lethalRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
postembryonic development variantRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
maternal sterileRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
postembryonic development variantRNAi:
WBRNAi00028805
Paper evidence: Rual JF et al., 2004
details
locomotion variantRNAi:
maternal sterileRNAi:
WBRNAi00040346
Paper evidence: Sonnichsen B et al., 2005
details
embryonic lethalRNAi:
WBRNAi00010618
Paper evidence: Kamath RS et al., 2003
details
maternal sterileRNAi:
WBRNAi00040345
Paper evidence: Sonnichsen B et al., 2005
details
sterileRNAi:
egg laying defectiveRNAi:
lethalRNAi:
postembryonic development variantRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
slow growthRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
embryonic lethalRNAi:
WBRNAi00040346
Paper evidence: Sonnichsen B et al., 2005
details
nematode phenotypeRNAi:
nematode phenotypeRNAi:
WBRNAi00040345
Paper evidence: Sonnichsen B et al., 2005
details
organism morphology variantRNAi:
protruding vulvaRNAi:
nematode phenotypeRNAi:
WBRNAi00010617
Paper evidence: Kamath RS et al., 2003
details
embryonic lethalRNAi:

Interaction-based phenotypes:

The following phenotypes are indirectly caused or affected by some perturbation of unc-77 in the context of a genetic interaction :

Phenotype Interactions Interaction Type Citations
evoked postsynaptic current variant21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77SyntheticYeh E et al., 2008
evoked postsynaptic current variant21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77A phenotypicYeh E et al., 2008
evoked postsynaptic current variant21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77DivergingYeh E et al., 2008
fainter21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77SyntheticYeh E et al., 2008
fainter21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77A phenotypicYeh E et al., 2008
fainter21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77DivergingYeh E et al., 2008
endogenous synaptic event frequency reduced21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77SyntheticYeh E et al., 2008
endogenous synaptic event frequency reduced21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77A phenotypicYeh E et al., 2008
endogenous synaptic event frequency reduced21ur-14100 : 21ur-2262 : 21ur-4260 : 21ur-4646 : 21ur-5158 : 21ur-7268 : 21ur-8078 : nca-2 : unc-77DivergingYeh E et al., 2008

Overexpression:
Overexpression of the unc-77 gene results in the following phenotypes.