FlyBase Allele Report: Dmel\fbl[1]

General Information

Symbol

Dmel\fbl¹

Species

D. melanogaster

Name

FlyBase ID

FBal0028192

Feature type

allele

Associated gene

Dmel\fbl

Associated Insertion(s)

P{PZ}fbl¹

Carried in Construct

Also Known As

fumble¹

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Afshar et al., 2001)

Mutagen

P-element activity

(Castrillon et al., 1993)

Progenitor genotype

Associated Insertion(s)

P{PZ}fbl¹

Cytology

Description

Allele components

Component

Use(s)

Inserted element

P{PZ}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

transposable_element_insertion_site

3L:20,384,453..20,384,453 [+]

(Afshar et al., 2001, Spradling et al., 1999, BDGP Project Members, 1994-1999, Castrillon et al., 1993)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 ( 1 )

Disease

Evidence

References

model of pantothenate kinase-associated neurodegeneration

CEA

(Rana et al., 2010, Wu et al., 2009, Bosveld et al., 2008)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of pantothenate kinase-associated neurodegeneration

is ameliorated by Hsap\PANK3^UAS.cWa

(Wu et al., 2009)

is ameliorated by Hsap\PANK4^UAS.cWa

(Wu et al., 2009)

is ameliorated by Hsap\PANK2^m.UAS

(Wu et al., 2009)

Comments on Models/Modifiers Based on Experimental Evidence ( 1 )

In fbl¹ pantothenate kinase-associated neurodegeneration disese model mutants usually die during pupal stage. The rare survivors show impaired locomotion and neurodegeneration.

(Wu et al., 2009)

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal behavior | female | recessive

(Afshar et al., 2001)

abnormal cytokinesis | male

(Afshar et al., 2001)

abnormal flight

(Bosveld et al., 2008)

abnormal locomotor behavior

(Wu et al., 2009)

abnormal locomotor behavior | adult stage

(Bosveld et al., 2008)

abnormal locomotor behavior | adult stage | progressive

(Rana et al., 2010)

abnormal locomotor behavior | larval stage

(Siudeja et al., 2011, Bosveld et al., 2008)

abnormal locomotor behavior | third instar larval stage

(Rana et al., 2010)

abnormal mating behavior | dominant

(Sun et al., 2025)

abnormal meiotic cell cycle (with fbl²)

(Afshar et al., 2001)

abnormal meiotic cell cycle (with fbl³)

(Afshar et al., 2001)

abnormal meiotic cell cycle | recessive

(Afshar et al., 2001)

abnormal neuroanatomy

(Wu et al., 2009)

chemical sensitive

(Bosveld et al., 2008)

female sterile

(Bosveld et al., 2008)

female sterile | recessive

(Afshar et al., 2001)

flightless

(Bosveld et al., 2008)

increased cell death | larval stage

(Bosveld et al., 2008)

lethal - all die before end of pupal stage

(Gutiérrez et al., 2010, Wu et al., 2009)

male sterile

male sterile | recessive

(Spradling et al., 1999)

partially lethal | recessive

(Siudeja et al., 2011)

radiation sensitive

(Bosveld et al., 2008)

short lived

(Srinivasan et al., 2015, Rana et al., 2010, Wu et al., 2009, Bosveld et al., 2008)

some die during pupal stage

(Gutiérrez et al., 2010, Wu et al., 2009)

sterile

(Wu et al., 2009)

uncoordinated | female | recessive

(Afshar et al., 2001)

visible

(Bosveld et al., 2008, Bosveld et al., 2008)

Phenotype Manifest In

adult brain

(Wu et al., 2009, Bosveld et al., 2008)

anterior crossvein

(Bosveld et al., 2008)

dorsal appendage | maternal effect

(Bosveld et al., 2008)

egg | maternal effect

(Bosveld et al., 2008)

flight muscle cell | progressive

(Rana et al., 2010)

larval brain

(Bosveld et al., 2008)

mitochondrion | adult stage

(Rana et al., 2010)

Nebenkern

(Wu et al., 2009, Castrillon et al., 1993)

Nebenkern derivative

(Afshar et al., 2001)

onion stage spermatid

(Wu et al., 2009)

ovary

(Wu et al., 2009, Bosveld et al., 2008)

posterior crossvein

(Bosveld et al., 2008)

retina | adult stage

(Wu et al., 2009)

spermatid

(Castrillon et al., 1993)

spermatid (with fbl²)

(Afshar et al., 2001)

spermatid & nucleus

(Afshar et al., 2001)

spermatocyte & aster (with fbl²)

(Afshar et al., 2001)

spermatocyte & aster (with fbl³)

(Afshar et al., 2001)

spermatocyte & centrosome

(Afshar et al., 2001)

spermatocyte & spindle

(Afshar et al., 2001)

spermatocyte & spindle (with fbl²)

(Afshar et al., 2001)

spermatocyte & spindle (with fbl³)

(Afshar et al., 2001)

testis

(Wu et al., 2009, Castrillon et al., 1993)

wing

(Bosveld et al., 2008)

Detailed Description

Statement

Reference

Lifespan of fbl¹/fbl¹ flies is significantly shorter than wild type; addition of coenzyme A (CoA) to food increases mutant lifespan from around 20 days to around 40 days.

(Srinivasan et al., 2015)

All male progeny collected from low zinc w¹¹⁸ mothers crossed to high/normal fbl¹ fathers are low in zinc. All female progeny from the same cross are high/normal in zinc. Male progeny from high/normal zinc females crossed to low zinc fbl¹ males are high/normal in zinc. This implies that a recessive X-linked mutation is affecting total body zinc accumulation, rather than the fbl¹ mutation.

(Afshar et al., 2013)

Homozygous larvae show reduced crawling ability compared to controls.

(Siudeja et al., 2011)

fbl¹ heterozygotes show a significant threefold increase in total Zn levels.

Under normal diet conditions approximately 55% of expected homozygous fbl¹ are found, suggesting that one third of homozygous fbl¹ larvae fail to initiate metamorphosis.

The addition of 5mM ZnCl[[2]] to the diet of fbl¹/+ flies results in a 40% increase in total zinc levels compared to controls with no Zn supplement. Controls with a 5mM ZnCl[[2]] supplemented diet exhibit a 55% increase in total Zn levels. A significant drop in expected fbl¹ homozygous pupae is observed when they are raised on high Zn (43% of expected), suggesting that Zn has a negative impact on larval development of fbl¹ homozygotes. The addition of 100υM TPEN to the diet of fbl¹ homozygous larvae does not significantly ameliorate their survival, despite reducing to less than half the levels of total Zn in adult fbl¹ heterozygous flies.

fbl¹ heterozygotes show no change in iron, manganese or copper levels.

(Gutiérrez et al., 2010)

fbl¹ mutant adults have shorter lifespan and show age-progressive flight muscle degeneration ('loose' appearance, ruptures), the mitochondria in the flight muscles of 12 day-old flies display severe morphological damage: they appear swollen, with damaged cristae and ruptured membranes.

fbl¹ mutants show locomotion defects: third instar larvae have decreased crawling abilities and the adults display reduced climbing abilities that rapidly decline further with age.

(Rana et al., 2010)

fbl¹ mutants die during the pupal stage with a few escapers managing to eclose and survive several days. Rare survivors exhibit impaired locomotion ability, infertility, and neurodegeneration in the brain and retina. Brain and retinal tissues display large vacuoles. The female ovary is dramatically reduced in size, and no mature sperm is evident in the male testis. In fbl¹ males, Nebenkern spermatids carry large Nebenkern and micronuclei at onion stage.

(Wu et al., 2009)

Homozygous females do not deposit eggs.

Homozygous ovaries dissected 48 hours after eclosion are poorly developed and do not contain eggs. Five day old homozygous ovaries contain eggs, which are small, ball-shaped and contain short dorsal appendages.

Production of neutral lipids is hardly detected in homozygous egg chambers.

Anterior cross vein and posterior cross vein formation is incomplete in homozygous wings, and mispositioned cross veins are found between veins L2 and L3.

Ectopic macrochaetae on the scutellum are not formed in homozygous flies.

(Bosveld et al., 2008)

Homozygous larvae show severely impaired locomotor activity (crawling) compared to controls.

(Bosveld et al., 2008)

7 day old homozygous flies show severe defects in flight ability and in the ability to climb in a negative geotaxis assay.

Homozygous flies have a reduced median lifespan (8 days) compared to control flies (50 days).

Homozygous flies often have held-out or (less frequently) held-up wings.

The brains of 14 day old homozygous adults contain vacuoles, suggesting neurodegeneration.

The level of triglycerides is reduced approximately 25% in 5 day old homozygous adults compared to controls.

Homozygous adults show a mild-sensitivity to H[[2]]O added to the medium under "wet starvation conditions".

Homozygous adults show increased sensitivity to 5% H[[2]]O[[2]], 100mM dithiothreitol and 20mM paraquat compared to control adults.

Homozygous larvae show reduced survival on medium containing 100mM cysteine compared to control larvae.

Homozygous third larval instar brains show a high incidence of abnormal mitotic chromosomes compared to controls.

Treatment with 20 Gy irradiation results in an increased incidence of abnormal mitotic chromosomes in homozygous third larval instar brains compared to controls.

Homozygous larval brains show an increased level of apoptosis compared to controls.

The survival rate of adults after exposure of larvae to 20Gy irradiation is reduced in homozygotes compared to wild-type flies.

(Bosveld et al., 2008)

fbl¹ males show defects in chromosome segregation and cytokinesis in the male germline. Homozygous females are uncoordinated. Approximately 10% of testis cysts in homozygous males contain spermatids with mitochondrial aggregates of abnormal size and shape and multinucleate nuclei of different size. Approximately 10% of homozygous primary spermatocytes have abnormal spindles at prometaphase or metaphase, having asymmetric and/or apolar microtubule structures and lacking actin structures. There is also a failure in centrosomal separation. Chromosomes are associated with only one half of the spindle in some spermatocytes. In some cases the actin contractile ring forms around the chromosomes at the midbody, indicating a defect in the timing of contractile ring formation or in chromosome segregation. At late telophase, cells containing two or more actin rings and associated cleavage furrows situated between distinct masses of chromosomes are seen, suggesting unequal partitioning of chromosomal masses and cytoplasm. 90% of spermatids in fbl¹/fbl² males undergo aberrant cell division and spermiogenesis (postmeiotic spermatid differentiation) is grossly defective. 80% of fbl¹/fbl² or fbl¹/fbl³ primary spermatocytes have spindle abnormalities, with the majority of spindles being multipolar. Anaphase and telophase stages are difficult to define in these testes, due to the severe defects in metaphase spindle organisation. In some less severely affected cells, two asters are seen at a single pole. Despite this lack of aster separation, these cells contain a contractile ring positioned over a central spindle.

(Afshar et al., 2001)

Spermatids have large nebenkern and micronuclei at onion stage. Hemizygotes have degenerating spermatocytes. Testes are short and nearly devoid of germinal content.

(Castrillon et al., 1993)

Spermatids with large Nebenkern and micronuclei at onion stage. Hemizygotes with deletion contain degenerating spermatocytes.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

fbl¹ has lethal | pupal stage phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

fbl¹ has short lived phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

fbl¹ has sterile phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

fbl¹ has lethal | pupal stage phenotype, suppressible by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has short lived phenotype, suppressible | partially by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, suppressible | partially by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has female sterile phenotype, suppressible | partially by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has lethal | pupal stage phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has short lived phenotype, suppressible | partially by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, suppressible | partially by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has female sterile phenotype, suppressible | partially by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has lethal | pupal stage phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK3^UAS.cWa

(Wu et al., 2009)

fbl¹ has short lived phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK3^UAS.cWa

(Wu et al., 2009)

fbl¹ has female sterile phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK3^UAS.cWa

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, suppressible | partially by Scer\GAL4^Act.PU/Hsap\PANK3^UAS.cWa

(Wu et al., 2009)

fbl¹ has lethal | pupal stage phenotype, suppressible by Hsap\PANK4^UAS.cWa/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has short lived phenotype, suppressible by Hsap\PANK4^UAS.cWa/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has female sterile phenotype, suppressible by Hsap\PANK4^UAS.cWa/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, suppressible | partially by Hsap\PANK4^UAS.cWa/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has chemical sensitive phenotype, suppressible by Sod1^+t2.4/Cat^tOa/Trxr1^+t10

(Bosveld et al., 2008)

NOT suppressed by

Statement

Reference

fbl¹ has short lived phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^c.UAS

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^c.UAS

(Wu et al., 2009)

fbl¹ has sterile phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^c.UAS

(Wu et al., 2009)

fbl¹ has male sterile phenotype, non-suppressible by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has male sterile phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has lethal | pupal stage phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has short lived phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has abnormal locomotor behavior phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has male sterile phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has male sterile phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK3^UAS.cWa

(Wu et al., 2009)

fbl¹ has male sterile phenotype, non-suppressible by Hsap\PANK4^UAS.cWa/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has lethal | pupal stage phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^c.UAS

(Wu et al., 2009)

Other

Statement

Reference

MTF-1^140-1R, fbl¹ has abnormal locomotor behavior phenotype

(Gutiérrez et al., 2010)

Phenotype Manifest In

Suppressed by

Statement

Reference

fbl¹ has adult brain phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

fbl¹ has retina phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

fbl¹ has testis phenotype, suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^m.UAS

(Wu et al., 2009)

NOT suppressed by

Statement

Reference

fbl¹ has adult brain phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has retina | adult stage phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has adult brain phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has retina | adult stage phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has adult brain phenotype, non-suppressible by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has retina | adult stage phenotype, non-suppressible by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

fbl¹ has testis phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^G411R.UAS

(Wu et al., 2009)

fbl¹ has testis phenotype, non-suppressible by Scer\GAL4^Act.PU/Hsap\PANK2^S241P.UAS

(Wu et al., 2009)

fbl¹ has testis phenotype, non-suppressible by Hsap\PANK2^T418M.UAS/Scer\GAL4^Act.PU

(Wu et al., 2009)

Enhancer of

Statement

Reference

fbl[+]/fbl¹ is an enhancer of wing margin phenotype of Bx²

(Bronstein et al., 2010)

NOT Enhancer of

Statement

Reference

fbl[+]/fbl¹ is a non-enhancer of scutellar bristle | increased number phenotype of Chi^e5.5

(Bronstein et al., 2010)

fbl[+]/fbl¹ is a non-enhancer of scutellar bristle | increased number phenotype of Ssdp^L7

(Bronstein et al., 2010)

NOT Suppressor of

Statement

Reference

fbl[+]/fbl¹ is a non-suppressor of scutellar bristle | increased number phenotype of Chi^e5.5

(Bronstein et al., 2010)

fbl[+]/fbl¹ is a non-suppressor of scutellar bristle | increased number phenotype of Ssdp^L7

(Bronstein et al., 2010)

Additional Comments

Genetic Interactions

Statement

Reference

Simultaneous co-expression of Sod^+t2.4, Cat^tOa and Trxr-1^+t10 restores survival of fbl¹/fbl¹ larvae on medium containing 100mM cysteine to wild-type levels.

(Bosveld et al., 2008)

Xenogenetic Interactions

Statement

Reference

Expression of Hsap\PANK2^m.Scer\UAS under the control of Scer\GAL4^Act.PU in a fbl¹ mutant background rescues the eclosion defects of fbl¹ flies, and the lifespan of these animals recovers to almost normal levels. Locomotor defects and infertility are also rescued in these animals. Retinal and brain morphology is normal in these animals at 12 days and 30 days old.

Expression of Hsap\PANK2^c.Scer\UAS under the control of Scer\GAL4^Act.PU does not rescue eclosion rate, lifespan, locomotion ability, and fertility defects of fbl¹ mutant flies.

Expression of Hsap\PANK2^{T418M.Scer\UAS} or Hsap\PANK2^{S241P.Scer\UAS} under the control of Scer\GAL4^Act.PU in a fbl¹ mutant background dramatically increased the eclosion rate. Ectopic expression of either line partially suppresses the impaired locomotion phenotype and short lifespan of fbl¹ mutant flies. Female fertility is restored in these animals but males are sterile and display abnormal spermatogenesis.

Expression of Hsap\PANK2^{G411R.Scer\UAS} under the control of Scer\GAL4^Act.PU does not alter eclosion rate of fbl¹ mutant flies, and does not increase lifespan or improve locomotion ability of fbl¹ mutant flies. Males are sterile and show abnormal spermatogenesis.

Expression of Hsap\PANK2^{T418M.Scer\UAS} under the control of Scer\GAL4^Act.PU in a fbl¹ mutant background results in a neurodegeneration phenotype. Adult brain and retinal tissue display large vacuoles at 12 days old.

Expression of Hsap\PANK2^{S241P.Scer\UAS} or Hsap\PANK2^{G411R.Scer\UAS} under the control of Scer\GAL4^Act.PU in a fbl¹ mutant background results in a neurodegeneration phenotype, with large vacuoles present in both tissues at 30 days post-eclosion.

Expression of Hsap\PANK3^Scer\UAS.cWa or Hsap\PANK4^Scer\UAS.cWa under the control of Scer\GAL4^Act.PU in a fbl¹ mutant background dramatically increases the eclosion rate of fbl¹ mutant flies, and the lifespan of these animals is much increased. Flies display normal climbing behaviour when young, however the climbing ability of these animals is less than 50% of control levels at 30 days. Female fertility is restored in these animals but male sterility is not restored.

(Wu et al., 2009)

Complementation and Rescue Data

Fails to complement

fbl⁰⁰⁷¹³

(BDGP Project Members, 1994-1999)

Rescued by

fbl¹ is rescued by Scer\GAL4^Act.PU/fbl^L.UAS

(Wu et al., 2009)

Partially rescued by

fbl¹ is partially rescued by Scer\GAL4^elav.PU/fbl^L.UAS

(Wu et al., 2009)

fbl¹ is partially rescued by fbl^L.UAS/Scer\GAL4^Ddc.PL

(Wu et al., 2009)

fbl¹ is partially rescued by fbl^L.UAS/Scer\GAL4^ChAT.7.4

(Wu et al., 2009)

Not rescued by

fbl¹ is not rescued by Scer\GAL4^Act.PU/fbl^S1.UAS

(Wu et al., 2009)

fbl¹ is not rescued by Scer\GAL4^Act.PU/fbl^S2.UAS

(Wu et al., 2009)

Comments

Expression of fbl^L.Scer\UAS under the control of Scer\GAL4^Act.PU rescues the eclosion defects of fbl¹ flies, and the lifespan of these animals recovers to almost normal levels. Locomotor and infertility defects are also rescued in these animals.

Expression of fbl^S1.Scer\UAS or fbl^S2.Scer\UAS under the control of Scer\GAL4^Act.PU in a fbl¹ mutant background does not rescue the lethality, shortened lifespan, locomotion behaviour, or infertility defects observed in fbl¹ mutants.

Expression of fbl^L.Scer\UAS under the control of Scer\GAL4^elav.PU in a fbl¹ mutant background rescues the eclosion defects, shortened lifespan and movement coordination defects of fbl¹ flies, but does not rescue infertility.

Expression of fbl^L.Scer\UAS in dopaminergic neurons under the control of Scer\GAL4^Ddc.PL partially rescues the eclosion rate, shortened lifespan, and locomotor defects of fbl¹ mutant flies.

Expression of fbl^L.Scer\UAS in cholinergic neurons under the control of Scer\GAL4^Cha.7.4 partially rescues the eclosion rate, shortened lifespan, and locomotor defects of fbl¹ mutant flies.

(Wu et al., 2009)

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

11777

P{PZ}fbl¹ ry⁵⁰⁶/TM3, ry^RK Sb¹ Ser¹

Kyoto

101721

P{PZ}fbl¹ ry⁵⁰⁶ / TM3, ry^RK Sb¹

Notes on Origin

Discoverer

Separable from: kug^fbl1.

(Horne-Badovinac et al., 2012)

The kug^fbl1 lesion was identified as a second hit on the fbl¹ chromosome.

(Horne-Badovinac et al., 2012)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (5)

Reported As

Symbol Synonym

dPANK¹

(Bosveld et al., 2008, Bosveld et al., 2008)

fbl⁰⁰⁴¹⁴

fbl¹

(Sun et al., 2025, Srinivasan et al., 2015, Horne-Badovinac et al., 2012, Siudeja et al., 2011, Bronstein et al., 2010, Rana et al., 2010, Christensen et al., 2009.2.28, Christensen et al., 2009.7.22, Wu et al., 2009, Bosveld et al., 2008, Bosveld et al., 2008, Christensen et al., 2008.4.15)

ms(3)00414

(Spradling et al., 1999)

Name Synonyms

fumble1

(Afshar et al., 2013, Gutiérrez et al., 2010)

Secondary FlyBase IDs

References (21)

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