FlyBase Allele Report: Dmel\sisA[1]

General Information

Symbol

Dmel\sisA¹

Species

D. melanogaster

Name

FlyBase ID

FBal0015671

Feature type

allele

Associated gene

Dmel\sisA

Associated Insertion(s)

Carried in Construct

Also Known As

sis-a, sis-a¹

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Erickson and Cline, 1998)

Mutagen

ethyl methanesulfonate

Progenitor genotype

Cytology

Description

Lys to Gln substitution within the DNA binding motif.

(Estes et al., 1995)

Amino acid replacement: K128E. Nucleotide substitution: A547G. Mutation is in a moderately conserved position of the DNA binding domain.

(Erickson and Cline, 1993)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:11,321,909..11,321,909 [-]

Nucleotide change:

A11321909G

Reported nucleotide change:

A6547G

Amino acid change:

K128E | sisA-PA

Reported amino acid change:

K128E

(Erickson and Cline, 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 ( 0 )

Disease

Evidence

References

Modifiers Based on Experimental Evidence ( 0 )

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

sc^10-1/sisA¹ female transheterozygotes have reduced viability, they are fully viable when they carry P{sc^sub}.

(Botella et al., 1996)

sc^sisB-1; l(1)sc^hb.PP and sisA¹; sc^hb.PP embryos lack posterior Sxl expression.

(Parkhurst et al., 1993)

Interacts with RpII140^wimp maternal effect.

(Parkhurst and Ish-Horowicz, 1991)

Female embryos hemizygous for sisA¹ show 100% lethality.

(Torres and Sanchez, 1991)

Homozygous females die but hemizygous males and heterozygous females fully viable; females die as embryos and larvae; rare morphologically normal and fertile escapers observed at lower temperatures. Single extant allele hypomorphic; locus also defined by dominant behavior of deficiencies and duplications. Dominant lethal for females simultaneously heterozygous for sis-b^- or Sxl^- or whose mothers are heterozygous for da^-. Magnitude of female-lethal dominant synergism sensitive to genetic background, but can be very high. Lethal interactions are generally less severe at lower culture temperatures. Constitutive allele, Sxl^M1, suppresses female lethality of sis-a homozygote or of any heterozygous combination of mutant alleles or deficiencies of these four genes. Duplication of Sxl⁺ also suppresses, but less effectively. Female-lethal interactions between sis-a and Sxl mutations display remarkably similar Sxl allele specificity to those between maternal da and zygotic Sxl mutations, indicating that da and sis-a disrupt the same aspect of Sxl regulation. Oogenesis normal for homozygous sis-a germ-line clones induced by mitotic recombination; no maternal effect in homozygous germ-line clones. Sexual phenotype of 2X:3A animals extremely sensitive to sis-a⁺ dose (more male at lower temperatures) and like da and Sxl^-, shows masculinizing interaction with autosomal male-specific lethal mutations but no increase in viability of escapers; nevertheless, sexual phenotype of homozygous sis-a clones generated by mitotic recombination normal. Female-lethal effects caused by decrease in sis-a function have their complement in male-lethal interactions caused by increase in sis-a function (duplications). Male lethality is increased as Sxl⁺ dose or sis-b⁺ dose is increased and is suppressed by loss-of-function Sxl mutations. The dose-dependent interactions of this gene with Sxl⁺ identify it as part of the numerator of what has been called the X/A balance, the primary sex-determination signal--a character it shares with sis-b.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable | maternal effect by mle¹/mle[+]

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable | maternal effect by msl-1^L60/msl-1[+]

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable | maternal effect by msl-2[+]/msl-2¹

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable | maternal effect by msl-3[+]/msl-3¹

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable by mof[+]/mof²

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable by roX1[+]/lncRNA:roX1^ex6

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype, enhanceable by lncRNA:roX2^unspecified/roX2[+]

(Gladstein et al., 2010)

Suppressed by

Statement

Reference

(Gladstein et al., 2010)

sisA¹/Df(1)N71 has lethal | female phenotype, suppressible by Sxl^M4

(Walker et al., 2000)

sisA²/sisA¹ has lethal | female phenotype, suppressible by Sxl^M4

(Walker et al., 2000)

sisA¹ has lethal | female phenotype, suppressible by dpn[+]/dpn³

(Barbash and Cline, 1995)

sisA¹ has lethal | female phenotype, suppressible by dpn[+]/dpn⁴

(Barbash and Cline, 1995)

sisA¹ has lethal | female phenotype, suppressible by dpn⁵/dpn[+]

(Barbash and Cline, 1995)

sisA¹ has lethal | female phenotype, suppressible by dpn[+]/dpn⁶

(Barbash and Cline, 1995)

sisA¹ has lethal | female phenotype, suppressible by dpn⁷/dpn[+]

(Barbash and Cline, 1995)

sisA¹ has lethal | female phenotype, suppressible by dpn⁸/dpn[+]

(Barbash and Cline, 1995)

sisA¹ has lethal | female phenotype, suppressible by sc^B5

(Erickson and Cline, 1991)

Other

Statement

Reference

msl-3¹, sisA[+]/sisA¹ has lethal | female | maternal effect phenotype

(Gladstein et al., 2010)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant | female phenotype

(Gladstein et al., 2010)

Bap60¹, sisA[+]/sisA¹, upd1^sisC-1/os[+] has partially lethal - majority die | dominant | maternal effect | female limited phenotype

(Möller et al., 2005)

Bap60¹, sisA[+]/sisA¹ has partially lethal - majority die | dominant | maternal effect | female limited phenotype

(Möller et al., 2005)

sc^T1/sc[+], sisA¹ has partially lethal - majority die phenotype

(Wrischnik et al., 2003)

sc[+]/sc^sisB-1, sisA¹ has partially lethal - majority die phenotype

(Wrischnik et al., 2003)

sc[+]/sc^sisB-2, sisA¹ has partially lethal - majority die phenotype

(Wrischnik et al., 2003)

sc[+]/sc^sisB-3, sisA¹ has partially lethal - majority die phenotype

(Wrischnik et al., 2003)

sc^M6, sisA[+]/sisA¹ has partially lethal - majority die | dominant phenotype

(Wrischnik et al., 2003)

sc^T1, sisA[+]/sisA¹ has partially lethal - majority die | dominant phenotype

(Wrischnik et al., 2003)

Dp(1;1)jnR1-A/+, sc^T2, sisA[+]/sisA¹ has lethal | dominant phenotype

(Wrischnik et al., 2003)

Dp(1;1)jnR1-A/+, sc^T3, sisA[+]/sisA¹ has partially lethal - majority die | dominant phenotype

(Wrischnik et al., 2003)

sc^sisB-1, sisA[+]/sisA¹ has partially lethal - majority die | dominant phenotype

(Wrischnik et al., 2003)

sc^sisB-2, sisA[+]/sisA¹ has partially lethal - majority die | dominant phenotype

(Wrischnik et al., 2003)

sc^sisB-3, sisA[+]/sisA¹ has partially lethal - majority die | dominant phenotype

(Wrischnik et al., 2003)

sc^M6/sc[+], sisA¹ has partially lethal - majority die phenotype

(Wrischnik et al., 2003)

sisA¹, upd1^sisC-5/upd1^sisC-1, upd1^t4.8 has lethal phenotype

(Sefton et al., 2000)

sisA¹, upd1^sisC-5/upd1^sisC-1 has lethal phenotype

(Sefton et al., 2000)

sisA[+]/sisA¹, upd1^sisC-5/upd1^sisC-1, upd1^t4.8 has lethal phenotype

(Sefton et al., 2000)

sisA[+]/sisA¹, upd1^sisC-5/upd1^sisC-1, upd1^t10 has partially lethal phenotype

(Sefton et al., 2000)

sisA[+]/sisA¹, upd1^sisC-5/upd1^sisC-1, upd1^t5.8 has partially lethal phenotype

(Sefton et al., 2000)

sisA¹, upd1^sisC-5/upd1^sisC-1 has lethal | dominant phenotype

(Sefton et al., 2000)

sisA¹/Df(1)N71, Sxl^M4 has viable phenotype

(Walker et al., 2000)

fl(1)35³⁵, sisA¹ has partially lethal | female phenotype

(Anand et al., 1998)

fl(1)35⁴⁶, sisA¹ has partially lethal | female phenotype

(Anand et al., 1998)

l(1)43⁴³, sisA¹ has partially lethal | female phenotype

(Anand et al., 1998)

Dvir\sisA^sisA.PK, sisA¹ has viable phenotype

(Erickson and Cline, 1998)

Phenotype Manifest In

Additional Comments

Genetic Interactions

Statement

Reference

sc^sisB-1 sisA¹/+ females show reduced viability compared to their male siblings.

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

The viability of sisA¹/+ females is significantly reduced if they also carry one maternally-derived copy of msl-3¹.

One paternally-derived copy of mof², roX1^ex6 or roX2^unspecified reduces the viability of sc^sisB-1 sisA¹/+ females.

The almost complete lethality of sc^sisB-1 sisA¹/+ females carrying a maternally-derived copy of msl-3¹ is significantly rescued (to 72.8% viability) by a maternally-derived copy of Sxl^M1.

(Gladstein et al., 2010)

Maternal heterozygosity for Bap60¹ reduces the viability of female offspring which are doubly heterozygous for sisA¹ upd1^sisC-1.

Maternal heterozygosity for Bap60¹ reduces the viability of female offspring which are heterozygous for sisA¹.

(Möller et al., 2005)

Does not interact with Sxl^dlf. Females doubly heterozygous for sisA¹ and either fl(1)35³⁵ or fl(1)35⁴⁶ show reduced viability compared to single heterozygous females. Females doubly heterozygous for l(1)43⁴³ and sisA¹ show reduced viability compared to single heterozygous females.

(Anand et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially complements

sisA⁴

(Walker et al., 2000)

Fails to complement

sisA²

(Walker et al., 2000)

sisA³