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General Information
Symbol
Dmel\S6kl-1
Species
D. melanogaster
Name
FlyBase ID
FBal0103996
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dS6kl-1, dS6Kl1, S6Kl1
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Imprecise excision of the P{PZ} element. Part of the first exon is removed, including part of the catalytic domain.

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
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

S6kl-1 homozygous somatic clones in third instar larval eye discs do not exhibit any delay in G1/S transition during the second mitotic wave, as mutant cells enter S phase in a similar region to control cells.

S6kl-1 mutant intestinal stem cell clones do not show any maintenance defects.

The autophagy defects observed in S6kl-1 mutant larval fat body cells are consistent with its suggested positive role in autophagy.

Bouton number/muscle area at the neuromuscular junction is normal in S6kl-1/Df(3L)CH18 third instar larvae. However, the mean bouton size is reduced approximately 40% compared to wild type. The number of active zones and the total synaptic area is significantly reduced at the mutant neuromuscular junction. Mean synaptic area is decreased more than active zone number, resulting in an increase in active zone density compared to wild type.

The mean amplitude of the spontaneous miniature excitatory postsynaptic potential (miniature EPSP) at the neuromuscular junction is normal in homozygous and S6kl-1/Df(3L)CH18 third instar larvae, although the miniature EPSP frequency is reduced in S6kl-1/Df(3L)CH18 third instar larvae compared to wild type. The mean amplitude of the evoked EPSP at the neuromuscular junction is significantly decreased in homozygous and S6kl-1/Df(3L)CH18 third instar larvae compared to wild type. There is also a correlated decrease in the quantal content in the mutant animals.

S6kl-1/S6k07084 mutant adult flies have a reduced body weight compared to heterozygous controls. Wing area is also reduced compared to controls.

Lipid content is increased in S6kl-1/S6k07084 mutant flies compared to controls. Carbohydrate content is similar to controls.

S6kl-1/S6k07084 mutant flies exhibit defective electroretinogram (ERG) readings.

Cholinesterase activity is significantly reduced in S6kl-1/S6k07084 mutant flies compared to controls.

S6kl-1 adult escapers exhibit a bent-down wing phenotype.

Homozygous dendrite arborization neuron clones show a of the dendritic arbors compared to wild type, with significant reductions in both the number and length of dendritic branches.

Eyes that are entirely comprised of S6kl-1 mutant clones (generated using WGMR.PG) are slightly smaller than in wild type.

Cells mutant for S6kl-1 show a strong decrease in TR-avidin uptake.

Ommatidial size in S6kl-1/S6kl-1 flies is reduced to 0.71 of wild-type.

Cells in S6kl-1 mutant clones in the eye are 0.65 times the size of their heterozygous neighbours.

Compared with wild-type pupae, S6kl-1 homozygous larvae are significantly reduced in size.

Mosaic eyes consisting primarily of mutant ommatidia are slightly smaller than normal due to decreases in ommatidium size.

The wing discs of S6kl-1 mutants are smaller than wild-type. The size of the nuclei in the endoreplicating salivary gland is smaller than wild-type.

The few homozygous escapers that do survive, emerge after a 5 day delay and live no longer than two weeks. They have a severe reduction in body size, with all body parts apparently affected to the same extent. Bristles are proportionate to the body size. The cell density is higher than wild-type (when wings and eyes are examined), the cells are almost 30% smaller, however the total number of cells remain normal. Wing discs are significantly smaller than wild-type and their cell size is on average smaller than wild-type. There is no apparent difference in the distribution of cell between wild-type and mutant within each phase of the cell cycle in larval discs. This is also the case when examined during early prepupal stage. The number of cells in S6kl-1 homozygous somatic clones are reduced compared to wildtype. Cell cycle times are 24+/-4 hours (compared to 12+/-1 in wild-type).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference

S6kl-1 has decreased body size | pupal stage phenotype, non-enhanceable by Tsc1[+]/Tsc1Q87X

Suppressed by
Statement
Reference

S6k[+]/S6kl-1, Tsc1Q87X has lethal phenotype, suppressible | partially by Tor2L1/Tor[+]

NOT suppressed by
Enhancer of
Statement
Reference

S6k[+]/S6kl-1 is an enhancer of visible phenotype of Scer\GAL4ey.PH, TctpdsRNA.UAS

NOT Enhancer of
Suppressor of
Statement
Reference

S6kl-1 is a suppressor of increased cell death phenotype of Rbf15aΔ, gig64

S6kl-1 is a suppressor of increased cell death phenotype of Rbf15aΔ, gig192

S6k[+]/S6kl-1 is a suppressor | partially of lethal | larval stage phenotype of Tsc1Q87X

S6k[+]/S6kl-1 is a suppressor | partially of lethal phenotype of Tor2L1/Tor[+], Tsc1Q87X

S6k[+]/S6kl-1 is a suppressor of visible phenotype of Pdk1A467V.UAS, Scer\GAL4ap-md544

NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Statement
Reference

S6k[+]/S6kl-1 is an enhancer of eye phenotype of Scer\GAL4ey.PH, TctpdsRNA.UAS

NOT Enhancer of
Suppressor of
Statement
Reference

S6kl-1 is a suppressor of eye disc | somatic clone phenotype of Rbf120a, gig192

S6kl-1 is a suppressor of eye | somatic clone phenotype of Rbf15aΔ, gig64

S6kl-1 is a suppressor of eye | somatic clone phenotype of Rbf15aΔ, gig192

S6kl-1/S6kl-1 is a suppressor of eye | somatic clone phenotype of Tsc1Q87X

S6k[+]/S6kl-1 is a suppressor of wing phenotype of Pdk1A467V.UAS, Scer\GAL4ap-md544

NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

S6kl-1 homozygous somatic clones also expressing ThorScer\UAS.cMa under the control of Scer\GAL4αTub84B.PL in third instar larval eye discs do not exhibit any delay in G1/S transition during the second mitotic wave, as mutant cells enter S phase in a similar region to control cells.

S6kl-1/+ suppresses the increase in excitatory junction current amplitude and quantal content seen in larvae NMJs expressing LrrkScer\UAS.cIa under the control of Scer\GAL4Mhc.PW.

S6kl-1 gig56 double mutant intestinal stem cell clones display a similar maintenance rate to that of wild-type intestinal stem cell clones, indicating that disruption of S6k can fully suppress the gig56-induced intestinal stem cell loss phenotype.

S6kl-1 gig56 double mutant intestinal stem cells do not exhibit obvious defects in lineage differentiation, as enteroendocrine cells and enterocyte cells are correctly differentiated in the clones.

Expression of Pdk1Scer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4VGlut-OK371 does not rescue the reduction in bouton size which is seen at the neuromuscular junction in S6kl-1/Df(3L)CH18 third instar larvae.

The basal level of E2f-dependent cell death normally present in Rbf120a mutant eye discs is suppressed in S6kl-1 mutant cells.

The ectopic cell death observed in Rbf120a gig192 is completely absent in Rbf120a gig192 S6kl-1 triple mutant cells.

The presence of a S6kl-1 background significantly decreases gig64/Rbf15aΔ induced cell death in the eye. In addition, much larger gig64/Rbf15aΔ double mutant clones are observed in adult eyes.

The presence of a S6kl-1 background significantly decreases gig192/Rbf15aΔ induced cell death in the eye. In addition, much larger gig192/Rbf15aΔ double mutant clones are observed in adult eyes.

Expression of Hr46ΔDBD.Scer\UAS under the control of Scer\GAL4ap-md544 suppresses the bent-down wing phenotype found in a S6kl-1 background.

The dendritic branches of ddaC neurons in TorΔP/+ ; S6kl-1/+ double heterozygous larvae have fewer branch points than wild-type controls.

Expression of RpL8dsRNA.Scer\UAS under the control of Scer\GAL4GMR.PF enhances the reduction in eye size seen in S6kl-1 mutant clones.

The reduction in eye size seen in animals expressing TctpdsRNA.Scer\UAS under the control of Scer\GAL4ey.PH is enhanced if they are also carrying S6kl-1/+.

Defects in autophagosome formation in starved Atg1EP3348 homozygous larvae are not rescued in a S6kl-1 heterozygous background. However, eclosion rates are increased in these animals in a dose-dependent manner and approximately 70% of Atg1EP3348, S6kl-1/+ animals eclose.

No difference in body weight between S6k07084/S6kl-1 scyl31/scyl31 double mutants and S6k07084/S6kl-1 single mutants is seen.

Eye overgrowth in RhebScer\UAS.cSa; Scer\GAL4GMR.PF animals is not suppressed by S6kl-1/S6kl-1, but ommatidia are smaller and less disorganized than those of RhebScer\UAS.cSa; Scer\GAL4GMR.PF alone, and the resulting eyes have a distinctive puckered appearance.

The large size and disorganisation of ommatidia in Scer\GAL4GMR.PF/+; RhebEP50.084/+ flies is suppressed by S6kl-1/S6kl-1. The partial dominant suppression of the large size and disorganisation of ommatidia in Scer\GAL4GMR.PF/+; RhebEP50.084/+ flies by Tor2L1 (ommatidia are 1.27 times wild-type size, and slightly disorganised) is enhanced by S6kl-1/+ (ommatidia 1.16 times wild-type size, and not disorganised).

The increase in cell size seen in somatic clones of gig192 in the eye is completely suppressed in double mutant somatic clones with S6kl-1. The decrease in cell size seen in somatic clones of S6kl-1 in the eye is completely suppressed in double mutant somatic clones with gig192.

The size reduction seen in S6kl-1 homozygous larvae is not significantly affected by heterozygosity for Tsc1Q87X. The second instar lethality of homozygous Tsc1Q87X is rescued to early pupal stages in a S6kl-1 homozygous background, however, the larvae are small and severely delayed in development. In contrast, in a S6kl-1/+ background Tsc1Q87X homozygous animals develop to early pupal stages with little developmental delay, and are significantly larger than wild type. The second instar lethality of homozygous Tsc1Q87X is rescued to adulthood (62%) or pupal stages (93%) by heterozygosity for both S6kl-1 and Tor2L1. The rescued animals are slightly larger than wild-type flies, with overall patterning appearing normal. The rescued females are semi-fertile when crossed to wild-type males, whereas the rescued males are fully fertile when crossed to wild-type females. Eye overgrowth caused by somatic clones of Tsc1Q87X in the developing eye and the increase in ommatidia size within the clones are suppressed in homozygous S6kl-1 animals. Eye overgrowth caused by somatic clones of Pten117 in the developing eye and the increase in ommatidia size within the clones are not suppressed in homozygous S6kl-1 animals.

The enlarged eye and ommatidia phenotype caused by expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF is not affected if the flies are also homozygous for S6kl-1.

Mosaic eyes consisting primarily of double mutant S6kl-1 Tsc1Q600X ommatidia show the S6kl-1 single mutant phenotype.

Xenogenetic Interactions
Statement
Reference

S6kl-1/+ fully suppresses the increase in excitatory junction current amplitude and quantal content seen in larvae NMJs expressing Hsap\LRRK2Scer\UAS.cVa under the control of Scer\GAL4Mhc.PW.

Expression of Hsap\RPL8DN.Scer\UAS under the control of Scer\GAL4GMR.PF enhances the reduction in eye size seen in S6kl-1 mutant clones.

The rough-eye phenotype observed in animals expressing Hsap\MAPTV337M.Scer\UAS under the control of Scer\GAL4GMR.PF is suppressed in a S6k07084/S6kl-1 background.

Complementation and Rescue Data
Fails to complement
Comments

The decrease in bouton size which is seen at the neuromuscular junction in S6kl-1/Df(3L)CH18 third instar larvae is fully rescued by expression of S6kScer\UAS.cCa under the control of either Scer\GAL4elav-C155 or Scer\GAL4VGlut-OK371, but is not rescued by expression of S6kScer\UAS.cCa under the control of Scer\GAL4C57.

Expression of S6kScer\UAS.cCa under the control of Scer\GAL4elav-C155 rescues the reduced active zone number and reduced reduced total synaptic area seen at the neuromuscular junction of S6kl-1/Df(3L)CH18 third instar larvae.

The decrease in bouton size which is seen at the neuromuscular junction in S6kl-1/Df(3L)CH18 third instar larvae is not rescued by expression of S6kKQ.Scer\UAS under the control of Scer\GAL4elav-C155.

The decrease in bouton size which is seen at the neuromuscular junction in S6kl-1/Df(3L)CH18 third instar larvae is rescued by expression of S6kSTDETE.Scer\UAS under the control of Scer\GAL4elav-C155 and the boutons are actually increased in size compared to wild type in the rescued animals.

The reduced active zone number and reduced reduced total synaptic area seen at the neuromuscular junction of S6kl-1/Df(3L)CH18 third instar larvae is also rescued by expression of S6kSTDETE.Scer\UAS under the control of Scer\GAL4elav-C155 (the numbers are actually increased in size compared to wild type in the rescued animals).

Expression of S6kScer\UAS.cWa under the control of Scer\GAL4Act5C.PP rescues the lethality associated with S6kl-1.

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Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (14)
References (32)