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General Information
Symbol
Dmel\Sin3A08269
Species
D. melanogaster
Name
FlyBase ID
FBal0008136
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
l(2)08269, Sin3Alof
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

Stated to be a P{lacW} insertion within an intron.

Insertion components
P{PZ}Sin3A08269
Product class / Tool use(s)
Encoded product / tool
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 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Homozygous Sin3A08269 embryos display a range of muscle phenotypes. Defects are observed in 100% of embryos and 100% of hemisegments. Early defects are not observed and a recognizable muscle pattern is generated. All die as embryos. Mature tendon cells are properly specified and positioned and embryos display a wild type cuticle pattern, indicating that ectodermal patterning is normal. Lateral transverse muscles (LTs 1-4) are often misshapen and frequently attach incorrectly; missing or unattached LTs are also frequently observed. Ventral acute muscles (VA1 and VA2) show less frequent defects, but muscle mis-attachment and mild changes in muscle shape are detected. Expression of 'identify genes' shows that the LT and VA muscles are specified correctly in Sin3A08269 mutants; myoblast fusion also occurs.

Sin3A08269 flies reared on 62.5, 125, and 250υM rotenone-supplemented food display a robust resistance to rotenone-induced early mortality after 3 and 7 days and show a significant improvement in the odds of survival as compared to wild-type flies at 62.5 and 125υM rotenone doses after 3 days and at 125υM rotenone dose after 7 days.

Sin3A08269 flies reared on 62.5, 125, and 250υM rotenone-supplemented food for 3 days exhibit a robust improvement in climbing ability and show a significant improvement in the odds of reaching the top section of the apparatus as compared to wild-type flies reared on 125υM rotenone-supplemented food.

Sin3A08269 flies reared on 10mM sodium butyrate and 10mM sodium butyrate and 62.5, 125, and 250υM10mM sodium butyrate and 62.5, 125, and 250υM rotenone-supplemented food show a significant improvement in the odds of survival as compared to flies reared on rotenone-supplemented food without sodium butyrate. There is no additive effect of sodium butyrate-supplementation in Sin3A08269 flies on rotenone-induced locomotor impairment.

Sin3A08269 flies reared on 125&ugrM rotenone-supplemented food show a significant dopamine deficiency as compared to vehicle-treated flies. However, Sin3A08269 flies reared on 125υM rotenone-supplemented food display a non-significant trend for moderately higher dopamine content as compared to wild-type flies reared on 125υM rotenone-supplemented food.

One copy of Sin3A08269 has no effect on hemocyte proliferation in third instar larvae.

The average number of crystal cells per embryo is reduced (to 14.1) in homozygous stage 13-14 embryos compared to wild type (36 +/- 2.2 cells on average).

Expression of Sin3A08269 under the control of Scer\GAL4GMR.PF does not result in a rough eye phenotype.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

Sin3A[+]/Sin3A08269 is an enhancer of visible | dominant phenotype of HP141

Sin3A[+]/Sin3A08269 is an enhancer of visible phenotype of RetMEN2B.GMR

Sin3A[+]/Sin3A08269 is an enhancer of visible phenotype of RetMEN2A.GMR

Sin3A[+]/Sin3A08269 is an enhancer of visible phenotype of RetGMR.PR

NOT Enhancer of
Statement
Reference

Sin3A[+]/Sin3A08269 is a non-enhancer of visible | dominant phenotype of EgfrE1

Suppressor of
NOT Suppressor of
Statement
Reference

Sin3A[+]/Sin3A08269 is a non-suppressor of visible | dominant phenotype of EgfrE1

Other
Statement
Reference
Phenotype Manifest In
Enhancer of
Statement
Reference

Sin3A[+]/Sin3A08269 is an enhancer of wing vein L5 phenotype of HP141

Sin3A[+]/Sin3A08269 is an enhancer of eye phenotype of Hsap\APPAβ42.GMR.Tag:SS(rPENK)

Sin3A[+]/Sin3A08269 is an enhancer of eye phenotype of RetMEN2B.GMR

Sin3A[+]/Sin3A08269 is an enhancer of eye phenotype of RetMEN2A.GMR

Sin3A[+]/Sin3A08269 is an enhancer of eye phenotype of RetGMR.PR

NOT Enhancer of
Statement
Reference

Sin3A[+]/Sin3A08269 is a non-enhancer of eye phenotype of EgfrE1

Suppressor of
NOT Suppressor of
Statement
Reference

Sin3A[+]/Sin3A08269 is a non-suppressor of eye phenotype of EgfrE1

Sin3A08269 is a non-suppressor of eye phenotype of Scer\GAL4hs.2sev, ttk69.UAS.Tag:HA

Other
Additional Comments
Genetic Interactions
Statement
Reference

Scer\GAL4Mef2.PR-mediated expression of KrScer\UAS.cHa in a Sin3A08269/+ background results in 55% of embryos reproducibly displaying a muscle transformation of VA1 to VA2.

Scer\GAL4Mef2.PR-mediated expression of araScer\UAS.cGa in a Sin3A08269/+ background results in embryos displaying aberrant muscle phenotypes, including an increased number of LT muscles.

Embryos trans-heterozygous for Sin3A08269 and either Kr1 KrmCD (a Kr loss-of-function allele) or Df(3L)iro-DFM3 (a deletion of ara and caup) do not show mesodermal defects.

The small, rough eye phenotype caused by expression of asf1Scer\UAS.cMa under the control of Scer\GAL4ey.PH is significantly suppressed by Sin3A08269/+.

The thickening of the wing veins that is seen in N55e11/+ flies is suppressed by Sin3A08269/+.

The truncation of wing vein L5 that is seen in HP141/+ heterozygotes is enhanced by Sin3A08269/+.

The severity of the mutant eye phenotype caused by expression of IswiK159R.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4ey.PH is enhanced by Sin3A08269.

EcRC300Y/Sin3A08269 transheterozygotes show normal viability and no visible phenotype.

The eye phenotype caused by expression of ttk69.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.2sev is not dramatically modulated by Sin3A08269.

Xenogenetic Interactions
Statement
Reference

One copy of Sin3A08269 moderately suppresses the hemocyte overproliferation seen in third instar larvae when Hsap\RUNX1::Hsap\RUNX1T1Scer\UAS.cSa is expressed under the control of Scer\GAL4Hml.Δ.

Sin3A08269 rescues the progressive loss of dorsomedial dopamine neurons in the brain seen in flies expressing either Hsap\SNCAScer\UAS.cFa or Hsap\SNCAA30P.Scer\UAS under the control of Scer\GAL4elav.PU.

The rough eye phenotype caused by expression of Hsap\MAPTV337M.Scer\UAS under the control of Scer\GAL4GMR.PF is not modified if the flies are also carrying Sin3A08269.

Sin3A08269/+ increases the viability of flies expressing Hsap\HTTQ93.ex1p.Scer\UAS under the control of Scer\GAL4elav-C155 from 29% to 69% and reduces the extent and rate of neurodegeneration seen in these flies.

Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (11)
References (25)