FlyBase Allele Report: Dmel\ben[1]

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.

(Ma et al., 2014)

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.

(Merkle et al., 2009)

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 ben^Scer\UAS.cUa in a ben¹ mutant background, using Scer\GAL4^OK307 and Scer\GAL80^ts.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.

(Uthaman et al., 2008)

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.

(Oh et al., 1994)

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.

(Edgecomb et al., 1993)

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.

(Muralidhar and Thomas, 1993)

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

(Venard and Stocker, 1991)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

ben¹ has abnormal oxidative stress response phenotype, suppressible by hep^UAS.cBa/Scer\GAL4^elav.PU

(Ma et al., 2014)

ben¹ has short lived phenotype, suppressible by hep^UAS.cBa/Scer\GAL4^elav.PU

(Ma et al., 2014)

NOT suppressed by

Statement

Reference

ben¹ has abnormal neurophysiology phenotype, non-suppressible by bsk^K53R.UAS/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

ben¹ has abnormal neuroanatomy phenotype, non-suppressible by bsk^K53R.UAS/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

Suppressor of

Statement

Reference

ben[+]/ben¹ is a suppressor | partially of visible phenotype of Scer\GAL4^GMR.PU, egr^UAS.cIa

(Ma et al., 2014)

ben¹ is a suppressor of visible phenotype of Scer\GAL4^pnr.PU, egr^UAS.cIa

(Ma et al., 2014)

ben[+]/ben¹ is a suppressor of neoplasia | somatic clone phenotype of Ras85D^V12.UAS, Scer\GAL4^FRT.Act5C, l(2)gl⁴

(Ma et al., 2014)

NOT Suppressor of

Statement

Reference

ben¹ is a non-suppressor of visible phenotype of Scer\GAL4^sev.PU, Tak1^UAS.cMa

(Ma et al., 2014)

ben¹ is a non-suppressor of visible phenotype of Scer\GAL4^sev.PU, hep^CA.UAS

(Ma et al., 2014)

Other

Statement

Reference

Scer\GAL4^GMR.PU, ben¹, egr^UAS.cIa has visible phenotype

(Ma et al., 2014)

Phenotype Manifest In

NOT suppressed by

Statement

Reference

ben¹ has giant fiber neuron phenotype, non-suppressible by bsk^K53R.UAS/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

ben¹ has mesothoracic tergotrochanter muscle motor neuron phenotype, non-suppressible by bsk^K53R.UAS/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

ben¹ has gap junction phenotype, non-suppressible by bsk^K53R.UAS/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

ben¹ has synapse phenotype, non-suppressible by bsk^K53R.UAS/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

Suppressor of

Statement

Reference

ben[+]/ben¹ is a suppressor | partially of eye phenotype of Scer\GAL4^GMR.PU, egr^UAS.cIa

(Ma et al., 2014)

ben¹ is a suppressor of scutellum phenotype of Scer\GAL4^pnr.PU, egr^UAS.cIa

(Ma et al., 2014)

ben[+]/ben¹ is a suppressor of anterior-posterior compartment boundary of the wing disc phenotype of Scer\GAL4^ptc.PU, scrib^GD11666

(Ma et al., 2014)

NOT Suppressor of

Statement

Reference

ben¹ is a non-suppressor of eye phenotype of Scer\GAL4^sev.PU, Tak1^UAS.cMa

(Ma et al., 2014)

ben¹ is a non-suppressor of eye phenotype of Scer\GAL4^sev.PU, hep^CA.UAS

(Ma et al., 2014)

Other

Statement

Reference

Scer\GAL4^GMR.PU, ben^+t6, ben¹, egr^UAS.cIa has eye phenotype

(Ma et al., 2014)

Additional Comments

Genetic Interactions

Statement

Reference

One copy of ben¹ partially suppresses the small eye phenotype seen in females expressing egr^Scer\UAS.cIa under the control of Scer\GAL4^GMR.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 egr^Scer\UAS.cIa is expressed under the control of Scer\GAL4^pnr.PU.

ben¹ has no effect on the rough eye phenotype seen when hep^CA.Scer\UAS is expressed under the control of Scer\GAL4^sev.PU.

ben¹ has no effect on the rough eye phenotype seen when Tak1^Scer\UAS.cMa is expressed under the control of Scer\GAL4^sev.PU.

Expression of hep^Scer\UAS.cBa under the control of Scer\GAL4^elav.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 Ras85D^V12.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 scrib^GD11666 is expressed along the anterior/posterior (A/P) compartment boundary of wing imaginal discs under the control of Scer\GAL4^ptc.PU.

(Ma et al., 2014)

Expression of bsk^{K53R.Scer\UAS} in a ben¹ mutant background does not suppress the giant fiber axonal overgrowth phenotype found in these mutants.

(Uthaman et al., 2008)

The giant fibre (GF) of Ubx^abx-1 Ubx^bx-3 Ubx^pbx-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.

(Muralidhar and Thomas, 1993)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

ben¹ is rescued by ben^+t6

(Ma et al., 2014)

ben¹ is rescued by ben^UAS.cUa/Scer\GAL4^shot-OK307

(Uthaman et al., 2008)

ben¹ is rescued by Scer\GAL4^c17/ben^UAS.cUa

(Uthaman et al., 2008)

ben¹ is rescued by ben^+t18

(Oh et al., 1994)

ben¹ is rescued by ben^+t6

(Oh et al., 1994)

ben¹ is rescued by ben^+t10

(Muralidhar and Thomas, 1993)

ben¹ is rescued by ben^+t35

(Muralidhar and Thomas, 1993)

ben¹ is rescued by ben^+t8

(Muralidhar and Thomas, 1993)

Not rescued by

ben¹ is not rescued by ben^UAS.cUa/Scer\GAL4^c42.2

(Uthaman et al., 2008)

ben¹ is not rescued by Scer\GAL4^{shakB.lethal.4.1}/ben^UAS.cUa

(Uthaman et al., 2008)

Comments

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

(Ma et al., 2014)

Expression of ben^Scer\UAS.cUa under the control of Scer\GAL4^OK307 rescues the ben¹ physiological and anatomical phenotypes.

Expression of ben^Scer\UAS.cUa under the control of Scer\GAL4^c17 rescues the ben¹ physiological and anatomical phenotypes on 83% of flies. This increases to 91% when two ben^Scer\UAS.cUa transgenes are used.

Pre-synaptic expression of ben^Scer\UAS.cUa under the control of Scer\GAL4^c42.2, 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 ben^Scer\UAS.cUa under the control of the postsynaptic Scer\GAL4^{shakB.lethal.4.1} driver, fails to rescue the ben¹ mutant phenotype.

(Uthaman et al., 2008)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

9565

w¹¹⁸ ben¹/C(1)A, y¹

Notes on Origin

Discoverer

Wyman and Thomas.

Comments

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

(Thomas and Wyman, 1984)

Allelic series of TDT phenotype: ben^P2/ben^P2 < ben^P2/Df(1)HA92 < ben¹/ben^P2 < ben¹/ben¹ = ben¹/Df(1)HA92.

(Edgecomb et al., 1993)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

ben¹

(Bai et al., 2020, Bai et al., 2018, Ma et al., 2014, Ma et al., 2012, Merkle et al., 2009, Uthaman et al., 2008)

Name Synonyms

Secondary FlyBase IDs

References (13)

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