FlyBase Allele Report: Dmel\sls[j1D7]

(Domsch et al., 2013, Kolmerer et al., 2000, Machado and Andrew, 2000, Zhang et al., 2000, Spradling et al., 1999, BDGP Project Members, 1994-1999)

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 ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates myopathy

modeled by cher^JF02077

(González-Morales et al., 2017)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

mitosis & nuclear chromosome

(Machado and Andrew, 2000)

mitosis & nuclear chromosome (with sls^e4)

(Machado and Andrew, 2000)

mitotic cell cycle

(Machado and Andrew, 2000)

mitotic cell cycle (with sls^e4)

(Machado and Andrew, 2000)

myofibril

(Zhang et al., 2000)

visceral muscle fiber | embryonic stage

(Zhang et al., 2000)

Detailed Description

Statement

Reference

sls^j1D7 heterozygous adults have an apparently normal morphology and are able to fly, as are able to sustain high frequency wing beat, as compared to controls.

(González-Morales et al., 2017)

sls^j1D7/sls^g65 pupae are thin.

(Labeau-Dimenna et al., 2012)

23.7% of nuclei in sls^e4/sls^j1D7 larval brain neuroblasts show chromosome undercondensation (under condensation of heterochromatin as well as euchromatin is seen). Additional mitotic defects such as premature sister chromatid separation, polyploidy, aneuploidy and chromosome breakage are also seen.

(Machado and Andrew, 2000)

Mutant embryos show grossly normal morphology, normal segmentation, normal epidermal denticle belts and normal patterning of the neuromusculature. They show greatly reduced movement compared to wild-type. Mature embryos show striking defects in individual muscle fibre morphology. The parallel myofilament array seen in wild-type muscles is disrupted and myofilaments are arranged irregularly, both longitudinally and transversely. The unit of a thick myosin filament surrounded by an array of thin actin filaments can form correctly, whereas the overall arrangement of myofilaments is largely disrupted.

(Zhang et al., 2000)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

sls^g65/sls^j1D7 has visible | pupal stage phenotype, non-enhanceable by tn[+]/tn^ΔA

(Labeau-Dimenna et al., 2012)

Enhancer of

Statement

Reference

sls[+]/sls^j1D7 is an enhancer of partially lethal - majority live phenotype of Scer\GAL4^Mef2.PU, cher^JF02077

(González-Morales et al., 2017)

sls[+]/sls^j1D7 is an enhancer of lethal | adult stage phenotype of Mlp84B^P20/Df(3R)dsx2M

(Clark et al., 2007)

NOT Enhancer of

Statement

Reference

sls[+]/sls^j1D7 is a non-enhancer of visible | pupal stage phenotype of tn^ΔA/tn¹

(Labeau-Dimenna et al., 2012)

Suppressor of

Statement

Reference

sls[+]/sls^j1D7 is a suppressor of lethal - all die before end of pupal stage phenotype of tn^MJO-348

(Domsch et al., 2013)

sls[+]/sls^j1D7 is a suppressor of decreased body size phenotype of tn^MJO-348

(Domsch et al., 2013)

Other

Statement

Reference

cher^EPSΔ5, sls[+]/sls^j1D7 has abnormal flight phenotype

(González-Morales et al., 2017)

cher^sko, sls[+]/sls^j1D7 has abnormal flight phenotype

(González-Morales et al., 2017)

Phenotype Manifest In

Enhancer of

Statement

Reference

sls[+]/sls^j1D7 is an enhancer of myofibril | adult stage phenotype of Scer\GAL4^Mef2.PU, cher^JF02077

(González-Morales et al., 2017)

sls[+]/sls^j1D7 is an enhancer of sarcomere | adult stage phenotype of Scer\GAL4^Mef2.PU, cher^JF02077

(González-Morales et al., 2017)

sls[+]/sls^j1D7 is an enhancer of pupal cuticle phenotype of Mlp84B^P20/Df(3R)dsx2M

(Clark et al., 2007)

Suppressor of

Statement

Reference

sls[+]/sls^j1D7 is a suppressor of visceral muscle fiber phenotype of tn^MJO-348

(Domsch et al., 2013)

sls[+]/sls^j1D7 is a suppressor of filamentous actin phenotype of tn^MJO-348

(Domsch et al., 2013)

Additional Comments

Genetic Interactions

Statement

Reference

sls^j1D7 heterozygotes also heterozygous for either cher^EPSΔ5 or cher^sko, but not cher^Q1042X, exhibit flight defects, since high frequency wing beat is only sustained for a few seconds, as compared to wild-type and single heterozygous controls; in both genetic background, however, there are no obvious sarcomere defects.

Heterozygosity for sls^j1D7 enhances the semi-lethality and the myofibril shredding defects (even leading to the loss of the sarcomere structure) resulting from the expression of cher^JF02077 under the control of Scer\GAL4^Mef2.PU.

(González-Morales et al., 2017)

Pupae trans-heterozygous for tn^MJO-348 and sls^j1D7 undergo proper pupal morphogenesis and eclosion. Notably, mutant pupae homozygous for tn^MJO-348 and heterozygous for sls^j1D7 are slim and show a statistically significant increase in length when compared to homozygous tn^MJO-348 pupae. This result indicates a suppression of the muscle contraction and morphogenetic defects that are associated with the tn^MJO-348 mutant phenotype.

(Domsch et al., 2013)

sls^j1D7/+ does not enhance the tn¹/tn^ΔA thin pupae phenotype.

sls^j1D7/+ enhances the Df(3R)Mlp84B^P8/Df(3R)dsx2M thin pupae phenotype.

tn^ΔA/+ does not enhance the sls^j1D7/sls^g65 thin pupae phenotype.

(Labeau-Dimenna et al., 2012)

sls^j1D7 heterozygosity greatly increases the adult lethality of Df(3R)Mlp84B^P8/Df(3R)dsx2M mutants. sls^j1D7 heterozygosity also exacerbates the pupal case elongation phenotype associated with Df(3R)Mlp84B^P8/Df(3R)dsx2M or Mlp84B^P20/Df(3R)dsx2M.

sls^j1D7 heterozygosity reduces the viability of Mlp84B^P20/Df(3R)dsx2M mutants to zero.

sls^j1D7 heterozygosity in a Df(3R)Mlp84B^P8/Df(3R)dsx2M mutant background leads to striking muscle abnormalities. Most muscle fibers are wavy and/or spindly in appearance. A significant number of fibers are torn or show some degree of fraying. Closer examination of the double mutants reveals a profound loss of sarcomeric structure of single muscle fibers from third instar fillet preparations. Neither Df(3R)Mlp84B^P8/Df(3R)dsx2M hemizygotes, nor sls^j1D7 heterozygotes on their own display any obvious structural abnormalities at the light microscopic level.

(Clark et al., 2007)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

10017

y¹ w^*; P{lacW}sls^j1D7/TM3, Sb¹

Kyoto

111002

y^d2 w¹¹¹⁸ P{ey-FLP.N}2 P{5xglBS-lacZ.38-1}TPN1; P{lacW}sls^j1D7 P{neoFRT}80B/TM6B, P{Car20y}TPN1, Tb¹

Notes on Origin

Discoverer

L. and Y. Jan.

Comments

Excision of the P{lacW} element can give viable revertants. Based on the lethal stage and antibody staining, sls alleles form the series: sls^S000201 (weakest), sls^B173, sls^C995, sls^j1D7, sls^B68, sls^C872 (strongest).

(Zhang et al., 2000)

Excision of the P{lacW} reverts the lethal phenotype.

(Machado and Andrew, 2000)

Complements: l(3)06265⁰⁶²⁶⁵.

(BDGP Project Members, 1994-1999)

External Crossreferences and Linkouts ( 1 )

Crossreferences

GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.

AJ238577

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

Ket^j1D7

(Zhang et al., 2000)

Titin¹⁰

(Machado and Andrew, 2000)

Titin^j1D7

(BDGP Project Members, 1994-1999)

l(3)j1D7

(Bullard et al., 2004, Kolmerer et al., 2000, Machado and Andrew, 2000, Spradling et al., 1999)

l(3)j1D7^j1D7

sls^j1D7

(Ariss et al., 2018, González-Morales et al., 2017, Labeau-Dimenna et al., 2012, Clark et al., 2007)

Name Synonyms

Secondary FlyBase IDs

References (12)

Report Sections

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