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General Information
Symbol
Dmel\ben1
Species
D. melanogaster
Name
FlyBase ID
FBal0001101
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C13998449T

Reported nucleotide change:

C490T

Reported nucleotide change:

C289T

Amino acid change:

P97S | ben-PA; P97S | ben-PB; P97S | ben-PC; P97S | ben-PD; P97S | ben-PE

Reported amino acid change:

P97S

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: P97S.

Nucleotide substitution: C289T.

Nucleotide substitution: C490T. Amino acid replacement: P97S.

Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
ameliorates  cancer
Comments on Models/Modifiers Based on Experimental Evidence ( 1 )
 

ben1 ameliorates tumor-like growth and invasion when Ras85DV12.Scer\UAS is expressed in l(2)gl4 mutant cells.

Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

ben1 mutant males exhibit a significantly compromised resistance against treatment of paraquat, a herbicide that induced the formation of reactive oxygen species. Lifespan is reduced in ben1 mutant flies.

Embryos derived from homozygous females mated to wild-type males fail to develop; 72% contain only one nucleus, 12% contain 2-8 nuclei ad the remaining 16% have more than 8 nuclei. Only 2% hatch. 72% of the embryos have one acentrosomal spindle. These single spindles appear to be mitotic rather than meiotic; their presence requires fertilisation, they are positioned deep within the egg interior where the first mitotic spindle normally resides, polar bodies are present (indicating completion of meiotic divisions) and centrosomes are occasionally seen near the spindle. 80% of the embryos have a majority of spindles that are barrel-shaped and/or lacking centrosomes. Misaligned chromosomes are often seen.

Embryos derived from ben1/Df(1)KA10 females mated to wild-type males fail to develop; 40% contain only one nucleus, 43% contain 2-8 nuclei ad the remaining 17% have more than 8 nuclei. None of these embryos hatch. 50% of the embryos have a majority of spindles that are barrel-shaped and/or lacking centrosomes.

ben1 mutant tergotrochanteral motorneurons exhibit abnormally long, variable response latencies and do not follow 1:1 at high-frequency stimulation in 88% of responses. ben1/Df(1)HA92 transheterozygotes exhibit mutant synaptic responses in 93% of cases.

ben1 mutants exhibit an incipient chemical and gap junctional synapse.

Targeted expression of benScer\UAS.cUa in a ben1 mutant background, using Scer\GAL4OK307 and Scer\GAL80ts.αTub84B reveals the first 24 hours of pupal development to be critical for ben function in synaptic growth, despite synaptic growth occurring later during development.

Homozygous flies appear lethargic and uncoordinated, and do not show normal climbing behaviour. Adults are capable of flight, but will not initiate flight when dropped from a height. Viability is reduced, with approximately 60% of pupae failing to eclose successfully and dying during emergence. The giant fibre (GF) drives the tergotrochanteral muscle (TTM) at abnormally long latencies and the response fails completely at moderate frequencies in homozygous flies. Stimulation of the dorsal longitudinal muscle (DLM), and the three dorsoventral muscles (DVM I, II and III) by the GF appears normal. The terminal bend of the GF is abnormal. Gynandromorph analysis suggests that the GF phenotype is determined by the genotype of the head, which contains the cell body of the giant axon. Homozygous flies prefer visible light over UV light in a choice test, in contrast to wild-type flies. Photoreceptor R7 cell rhabdomeres appear deformed and displaced, and rhabdomeres of other photoreceptor cells may also show less severe abnormalities. The arrangement of the optic cartridges within the lamina is completely disrupted. Photoreceptor axons which reach the medulla make shallow disordered projections into it, and photoreceptor axon projections appear irregular and disordered after exiting the optic stalk.

TDT attachment sites vary. The muscle may be found in the wild type position, posterior to the intrascutal suture and displaced medially, anterior to the intrascutal suture or missing entirely. Muscle may also be reduced in size or split dorsally attaching to two separate sites on the scutum. Cytology of the TDT is also altered, muscles may have fibres that are swollen and stain abnormally, other fibres may have large, axially aligned holes. Attachment pattern of the DVMs is also altered. DVMs remain within their respective attachment regions or extend into the region normally occupied by an adjacent DVM. DVMs may be entirely missing. Many flies fail to eclose, dying during late pupal stages. Flies that do eclose show impaired motility. Flies can get stuck in their food, falling into the food causes their femurs to become swollen and bent.

Giant fibre (GF) fails to extend laterally along the tergotrochanteral jump muscle motorneuron (TTMmn) and instead terminates at the midline where it synapses with the peripherally synapsing interneuron (PSI). This results in a lack of direct synaptic connection between the GF and TTMmn.

Ethanol is capable of evoking a walk response at concentrations lower than 10%.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT suppressed by
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
NOT suppressed by
Suppressor of
NOT Suppressor of
Statement
Reference

ben1 is a non-suppressor of eye phenotype of Scer\GAL4sev.PU/Scer\GAL4sev.PU, Tak1UAS.cMa

ben1 is a non-suppressor of eye phenotype of Scer\GAL4sev.PU/Scer\GAL4sev.PU, hepCA.UAS

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

One copy of ben1 partially suppresses the small eye phenotype seen in females expressing egrScer\UAS.cIa under the control of Scer\GAL4GMR.PU. ben1/Y fully suppresses the small eye phenotype. This suppression is reverted upon expression of ben+t6.

ben1/Y fully suppresses the scutellum phenotype seen when egrScer\UAS.cIa is expressed under the control of Scer\GAL4pnr.PU.

ben1 has no effect on the rough eye phenotype seen when hepCA.Scer\UAS is expressed under the control of Scer\GAL4sev.PU.

ben1 has no effect on the rough eye phenotype seen when Tak1Scer\UAS.cMa is expressed under the control of Scer\GAL4sev.PU.

Expression of hepScer\UAS.cBa under the control of Scer\GAL4elav.PU fully rescues the reduced oxidative stress resistance and shortened lifespan seen in ben1 mutant males.

One copy of ben1 partially suppresses the growth and invasion of the tumors seen when Ras85DV12.Scer\UAS is expressed in l(2)gl4 mutant cells in eye-antennal discs using the ey-FLP/MARCM system.

One copy of ben1 suppresses the cell migration seen when scribGD11666 is expressed along the anterior/posterior (A/P) compartment boundary of wing imaginal discs under the control of Scer\GAL4ptc.PU.

Expression of bskK53R.Scer\UAS in a ben1 mutant background does not suppress the giant fiber axonal overgrowth phenotype found in these mutants.

The giant fibre (GF) of Ubxabx-1 Ubxbx-3 Ubxpbx-1/Df(3R)P2 mutants makes a midline tuft and extends a lateral process to T2 and T3 segment. In the presence of ben1 the GF is capable of extending a process into the T3 segment but no lateral processes from the midline. R7 rhabdomeres are reduced in size and often misplaced, outer rhabdomeres are loosely packed maintaining position further from the centre of the ommatidia. The ordered arrangement of photoreceptor neuron axons entering the lamina is disrupted. Also the medula is abnormally rotated in relation to the lamina.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of ben+t6 rescues the reduced oxidative stress resistance and shortened lifespan seen in ben1 mutant males.

Expression of benScer\UAS.cUa under the control of Scer\GAL4OK307 rescues the ben1 physiological and anatomical phenotypes.

Expression of benScer\UAS.cUa under the control of Scer\GAL4c17 rescues the ben1 physiological and anatomical phenotypes on 83% of flies. This increases to 91% when two benScer\UAS.cUa transgenes are used.

Pre-synaptic expression of benScer\UAS.cUa under the control of Scer\GAL4c42.2, which turns on expression in the later half of pupal development when the giant fiber would be undergoing additional growth after having made its synapse in wild-type specimens, fails to rescue the ben1 physiological and anatomical phenotypes.

Expression of benScer\UAS.cUa under the control of the postsynaptic Scer\GAL4shakB.lethal.4.1 driver, fails to rescue the ben1 mutant phenotype.

Targeted expression of benScer\UAS.cUa in a ben1 mutant background, using Scer\GAL4OK307 and Scer\GAL80ts.αTub84B reveals the first 24 hours of pupal development to be critical for ben function in synaptic growth, despite synaptic growth occurring later during development.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Wyman and Thomas.

Comments
Comments

The defect in the pathway responsible for the abnormal TTM muscle response is at the GF-TTM motor neuron junction.

Allelic series of TDT phenotype: benP2/benP2 < benP2/Df(1)HA92 < ben1/benP2 < ben1/ben1 = ben1/Df(1)HA92.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (13)