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General Information
D. melanogaster
FlyBase ID
Feature type
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
sis-bsc3-1, sc3-1
Nature of the Allele
Mutations Mapped to the Genome
Additional Notes
point mutation
Nucleotide change:


Amino acid change:

K136term | sc-PA

Reported amino acid change:



scsisB-1 contains a point mutation and a 12kb tandem duplication containing the scsisB-1 allele and the adjacent wild type l(sc) transcription unit. Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
Progenitor genotype
Nature of the lesion

The chromosome carries a tandem duplication (approximately 12kb) which includes a mutated form of sc (each copy carries the amino acid replacement K136term) and the adjacent wild-type l(1)sc transcription unit.

Expression Data
Reporter Expression
Additional Information
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Modifiers Based on Experimental Evidence ( 0 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description

At 18oC 76% of expected scsisB-2 homozygotes survive to adulthood, but this drops to 35% when these animals are raised at 25oC. 50-89% of scsisB-1 homozygous adults lack upper humeral and anterior orbital bristles. With variable penetrance, scsisB-1/In(1)sc8Lsc4R adults lack ocellar, anterior orbital, posterior orbital, postvertical, upper humeral, anterior supraalar, notopleural, posterior postalar, lower humeral and presutral bristles. With variable penetrance scsisB-1/Df(1)sc19 adults lack all head bristles apart from the posterior vertical bristles, and all bristles of the dorsal thorax apart from the posterior notoplural, posterior dorsocentral and scutellar bristles.

Temperature-sensitive mutation.

Embryonic lethality of females rescued by maternal ectopic expression of ac or l(1)sc. Maternal ac or sc can rescue scsisB-1 females.

Original hypomorphic allele recovered as a reversion of sc3 to nearly wild-type ac and sc phenotype in hemizygote and homozygote. Locus also characterized by dominant effects of deficiencies and duplications of the ASC region and later by mutant alleles sc10-1 and acHw-49c that affect ASC functions more than scsisB-1 functions. scsisB-1 reduces viability of homozygous females and hemizygous females are lethal; yet hemizygous males fully viable. Dominant synergistic female-specific lethal interactions with loss-of-function alleles of Sxl, sisA, and/or maternal da; magnitude of viability effects depends on genetic background and inversely correlates with background effects on male-lethal effects; interactions temperature-dependent, generally more extreme at higher temperatures. Female viability effects suppressed by gain-of-function SxlM1 allele and by duplications of Sxl+ or sisA+. Duplication of scsisB-1+ male-lethal in combination with duplication of Sxl+ and/or sisA+, more so at lower temperatures. Male lethality of duplication combinations suppressed by Sxl-. Phenotype of 2X;3A intersexes strongly dependent on dose of scsisB-1+. The dose-dependent interactions of this gene identify it as a positive regulator of Sxl+ and part of the numerator of what is referred to as the X/A balance, the primary sex-determination signal. This is a character it shares with sisA. RK2.

Temperature shift experiments showed that lowering sc activity in the presence of extra copies of dpn+ results in the death of females but not males.

The viability of homozygous females ranges from 100% at 18oC to less than 1% at 29oC.

Flies show a mild bristle phenotype. Sex determination is affected much more strongly by scsisB-1 than is neurogenesis, and the two aspects show different temperature dependencies. Temperature sensitive period for feamle lethal affect corresponds to peak of sc expression between nuclear cycles 9 and 14 in the embryo.

Interacts with RpII140wimp maternal effect.

80% of female scsisB-1/sc10-1 embryos die. All female scsisB-1/sc10-1 embryos heterozygous for Sxlf1 die. Female embryos heterozygous for scsisB-1 and Sxlf1, and deficient for one copy of sisA show 75% lethality.

Homozygous females show reduced viability hemizygous female lethal.

External Data
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by

msl-3[+]/msl-31, scsisB-1, sisA[+]/sisA1 has lethal | dominant | female | maternal effect phenotype, suppressible | maternal effect | partially by SxlM1/Sxl[+]

scsisB-1 has lethal | female phenotype, suppressible by dpn[+]/dpn3

scsisB-1 has lethal | female phenotype, suppressible by dpn[+]/dpn4

scsisB-1 has lethal | female phenotype, suppressible by dpn5/dpn[+]

scsisB-1 has lethal | female phenotype, suppressible by dpn[+]/dpn6

scsisB-1 has lethal | female phenotype, suppressible by dpn7/dpn[+]

Suppressor of

scsisB-1 is a suppressor | partially of lethal | female limited phenotype of MycP1

scsisB-1 is a suppressor | partially of lethal | female limited phenotype of Mycdm-1

scsisB-1 is a suppressor | partially of lethal | female limited phenotype of MycP0

Phenotype Manifest In
NOT suppressed by

scsisB-1 has phenotype, non-suppressible by su(Hw)2

Suppressor of

scsisB-1 is a suppressor | partially of macrochaeta | ectopic phenotype of hhbar3

Additional Comments
Genetic Interactions

Approximately 24% of scsisB-1 dm1 trans-heterozygous female offspring from dm1 fathers mated to scsisB-1 females survive.

Approximately 90% of scsisB-1 dmP0 trans-heterozygous female offspring from dmP0 fathers mated to scsisB-1 mothers survive.

Approximately 76% of scsisB-1 dmP1 trans-heterozygous female offspring from dmP1 fathers mated to scsisB-1 mothers survive.

scsisB-1 sisA1/+ females show reduced viability compared to their male siblings.

One maternally-derived copy of either mle1, msl-1L60, msl-21 or msl-31 significantly reduces the viability of scsisB-1 sisA1/+ females so that they show almost complete lethality. One paternally-derived copy of either mle1, msl-1L60, msl-21 or msl-31 significantly reduces the viability of scsisB-1 sisA1/+ females, although this zygotic effect is generally weaker than the maternal one.

The viability of scsisB-1/+ females raised at the non-permissive temperature of 29[o]C is significantly reduced if they also carry one maternally-derived copy of msl-31.

One paternally-derived copy of mof2, roX1ex6 or roX2unspecified reduces the viability of scsisB-1 sisA1/+ females.

The almost complete lethality of scsisB-1 sisA1/+ females carrying a maternally-derived copy of msl-31 is significantly rescued (to 72.8% viability) by a maternally-derived copy of SxlM1.

Ectopic macrochaetae on the scutellum of hhbar3 homozygotes is only very weakly suppressed by hemizygous scsisB-1.

Xenogenetic Interactions
Complementation and Rescue Data
Partially rescued by

scsisB-1 is partially rescued by scB6

scsisB-1 is partially rescued by scB7

scsisB-1 is partially rescued by scB5

Not rescued by

Rescue statements based on female specific lethality. Bristle phenotype is not rescued by sc+ transgenes.

Expression of schs.PR during the first two hours of development rescues female scsisB-1/sc10-1 embryos.

Images (0)
Stocks (3)
Notes on Origin

Revertant. \partial


The temperature sensitive period begins at nuclear cycle 9 and ends at the beginning of nuclear cycle 14.

Originally designated "sc3-1" by Sturtevant, renamed sis-b by Cline.

Lethal phenotype is due to failure to properly activate Sxl-Pe.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
References (25)