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General Information
Symbol
Dmel\SxlM1
Species
D. melanogaster
Name
FlyBase ID
FBal0016703
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
SxlM#1, SxlM
Mutagen
Nature of the Allele
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

Insertion of a 9.5kb roo element 674bp downstream of male specific exon 3; 249bp upstream of exon 4. The roo insertion is transcribed in the opposite direction to Sxl.

roo insertion near the sex-specific exon.

Insertion of a roo element.

Insertion of 9kb roo element into Sxl, approximately 10kb distal to the site of P-element insertion in SxlfPb.

partially constitutive due to roo insert near male-specific exon roo insertion

Insertion components
roo{}SxlM1
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

SxlM1,fPw+c suppresses the dominant male-specific lethality of SxlM1.

SxlM1,fΔ33 suppresses the dominant male-specific lethality of SxlM1.

The SxlM alleles differ in their ability to bypass the X:A signal. SxlM4 is more effective than SxlM3, is more effective than SxlM1, at suppressing female-specific zygotic lethality of sisA and scsisB mutations.

In males and females SxlM1 acts constitutively and is unaffected by the presence or absence of maternal her function. Presence of SxlM1 restores her1/hermat-1 female viability, males are inviable.

At room temperature snf1 SxlM1 males are seldom recovered, at 18oC 30% males are viable.

SxlM1 shows wild type dosage compensation in run25 phenotype assay.

SxlM1 suppresses the lethality of SxlfP7B0/Df(1)N19, Df(1)N71/Df(1)N19 and Df(1)svr/Df(1)N19 females.

SxlM1/X ; traunspecified/traunspecified larvae have gonads that are indistinguishable from XX ; traunspecified/traunspecified larvae. SxlM1/X ; traunspecified/traunspecified adult pseudomales often have degenerating cells in the testes. Germ cells in these flies can be either oogenic or spermatogenic (a single animal contains only oogenic or spermatogenic testes, not both).

Partially suppresses the lethality of homozygous fl(2)d1 and fl(2)d1/fl(2)d2 females. The lethality of SxlM1 males is partially suppressed in homozygous fl(2)d1 and fl(2)d1/fl(2)d2 flies.

Female sterility can be suppressed by SxlM1. Hemizygous male lethality can be partially suppressed by snf1.

fl(2)d1/fl(2)d1 SxlM1/+ adult females have normal viability in contrast to the reduced viability of fl(2)d1/fl(2)d1 adult females. Homozygous fl(2)d1 females are inseminated less than wild-type females, this phenotype is suppressed by SxlM1. Homozygous fl(2)d1 females developing at 18oC are sterile. This sterility is suppressed by SxlM1.

Approximately 85% of homozygous female sc10-1 embryos die. This lethality is completely rescued by one copy of SxlM1.

Male lethality is due to failure of dosage compensation.

SxlM1 heterozygotes that are also mutant for tra and are chromosomally female (XX) are transformed into "pseudomales". The gonads form testes, 22.5% of which are non-gametogenic, containing degenerated germ cells and debris or gonial cells whose sex could not be determined. The remaining 77.5% were gametogenic, containing oogenic stages which were arrested at stages S3-S6. Triploid intersexes with a chromosome ratio of 2X:3A are phenotypically female, but sterile in SxlM1 heterozygotes. The gonads form ovaries in which the germ cells invariably enter the oogenic pathway and usually become mature eggs, but eggs are never laid. Triploid intersexes with a chromosome ratio of 2X:3A are transformed to pseudomales in SxlM1 heterozygotes which are also tra mutants. The gonads form well developed and nicely coiled testes, which are mostly filled with spermatogenic germ cells which were usually arrested at the spermatocyte stage.

Homozygotes die as young larvae. Triploid intersexes carrying SxlM1 complete adult development but fail to eclose. Triploid intersexes that are carrying SxlM1 develop as phenotypic females.

Unconditionally lethal to males, even in the presence of a Sxl+ duplication. Retains normal level of

female function as evidenced by full viability and

fertility of homozygous and hemizygous mutant females.

Recovered by virtue of ability to bypass the normal

requirement by females for maternally supplied da+

product, a positive regulator of Sxl+; however,

bypass is incomplete at higher temperatures. Phenotype

in both sexes results from expression of Sxl+ female

sex determination and dosage compensation functions

largely (though not completely) independently of the

normal controls. This is shown by the observation that

induction of mutations in cis that suppress dominant,

male-specific lethality is invariably associated with

a corresponding reduction in Sxl+ female-specific

activities and the dominant da maternal-effect bypass

phenotype. SxlM1 is lethal to most gynandromorphs by

the pharate-adult stage, disrupting the development of

their haplo-X tissue in a cell-autonomous fashion;

mutant haplo-X tissue in gynandromorphs is often, but

not always, feminized. This variable penetrance of the

sex transformation suggests a residual level of

control by the X/A balance. SxlM1 feminizes triploid

intersexes, killing them as pharate adults, while

suppressing B and Hw alleles in a fashion consistent

with expectations for constitutive expression of

normal female dosage-compensation functions. Analysis

of effects on the dosage compensation of the very

early acting segmentation gene, run, suggests that

constitutive expression of female functions is not

observed prior to the time when the later Sxl promoter

is required and RNA processing control is known to be

operating. Since run dosage compensation during this

period does require functioning of maternal da+,

zygotic Sxl+ and the X/A balance, the ability of

SxlM1 to bypass these controls during later stages

of development would seem to indicate that the effect

of the mutant lesion it carries is on Sxl-RNA

splicing, a process that these other Sxl+ regulators

may only affect indirectly. The position of the

SxlM1 mutant lesion in the vicinity of the

male-specific exon is suggestive in this connection.

Variable expressivity of this mutant allele may

underlie two additional observations: (1)

SxlM1 male lethality can be suppressed by

snf, yet snf female sterility can be

suppressed by SxlM1 and (2) transplants of SxlM1/Y

and SxlM1/+ germ cells show that although the allele

does not appear to interfere with spermatogenesis in

testes, it blocks the otherwise masculinizing effect

of testicular somatic tissue on diplo-X (female) germ

cells.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

SxlM1 has lethal | male phenotype, suppressible | cold sensitive by snf1

SxlM1 has lethal | male phenotype, suppressible | heat sensitive by snf1

SxlM1 has lethal | male phenotype, suppressible by vir2f/vir22

SxlM1 has lethal | male phenotype, suppressible by vir23/vir2f

SxlM1 has lethal | male phenotype, suppressible by vir2f/Df(2R)vir15

SxlM1 has lethal phenotype, suppressible by snf1

NOT suppressed by
Statement
Reference

SxlM1 has lethal | male phenotype, non-suppressible by bbflex-2

Suppressor of
Statement
Reference

SxlM1/Sxl[+] is a suppressor | maternal effect | partially of lethal | dominant | female | maternal effect phenotype of msl-3[+]/msl-31, scsisB-1, sisA[+]/sisA1

SxlM1 is a suppressor of lethal | female phenotype of snf1

SxlM1 is a suppressor of female sterile phenotype of otu11

SxlM1 is a suppressor of lethal | male phenotype of schb.PP

SxlM1 is a suppressor of lethal | female phenotype of hhb.PP

NOT Suppressor of
Statement
Reference

SxlM1 is a non-suppressor of lethal | female | larval stage phenotype of virunspecified/vir3

SxlM1 is a non-suppressor of lethal | female | larval stage phenotype of virunspecified/vir4

SxlM1 is a non-suppressor of lethal | female | larval stage phenotype of virunspecified/vir5

SxlM1 is a non-suppressor of lethal | female | larval stage phenotype of virunspecified/vir6

SxlM1 is a non-suppressor of lethal | female | larval stage phenotype of virunspecified/vir7

SxlM1 is a non-suppressor of lethal | female | larval stage phenotype of virunspecified/virts

SxlM1 is a non-suppressor of female sterile phenotype of otu13

SxlM1 is a non-suppressor of female sterile phenotype of otu10

SxlM1 is a non-suppressor of female sterile phenotype of otu2

Other
Phenotype Manifest In
Suppressed by
Statement
Reference

SxlM1 has phenotype, suppressible by snf1

Suppressor of
Statement
Reference

SxlM1 is a suppressor of ovary phenotype of otu2

SxlM1 is a suppressor of ovary phenotype of otu13

SxlM1 is a suppressor of ovary phenotype of otu10

NOT Suppressor of
Statement
Reference

SxlM1 is a non-suppressor of ovary phenotype of ovoD1rv23

SxlM1 is a non-suppressor of ovary phenotype of ovoD1rv22

Other
Additional Comments
Genetic Interactions
Statement
Reference

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.

The almost complete lethality of SxlfP7B0/+ females carrying a maternally-derived copy of msl-31 is significantly rescued (to 98.7% viability) by a maternally-derived copy of SxlM1.

SxlM1 suppresses snf1 female sterility at 18[o] and 25[o]C, while snf1 suppresses male lethality only at 18[o]C.

Viable SxlM1 bbflex-2 double mutant males have not been recovered. snf1 partially suppresses SxlM1 male lethality; snf1 SxlM1 double mutant males are viable at 18oC but are not recovered at 25oC. The temperature sensitive lethality of snf1 SxlM1 males is still seen if they are also mutant for bbflex-2; triple mutant males are recovered at 18oC, but not at 25oC.

FlyBase curator comment: subsequent publication (FBrf0134557) calls into question the validity of the genetic interaction between bbflex-2 and SxlM alleles (SxlM1 and SxlM4) stated in FBrf0111803. The suppression of the male lethality by bbflex-2 is slightly temperature dependent with fewer males surviving at 29oC than at 25oC. The resulting males are viable and fertile with no evidence of transformation.

Ovaries of ovoD1rv23/ovoD1rv22 females contain germline chambers in less than 20% of cases. The phenotype is not affected if the females are also carrying SxlM1. ovoD1rv22/ovoD1rv22; mle1/mle1 ovaries most often contain germ cells of male morphology rather than female morphology. This phenotype is partially suppressed by SxlM1; ovaries more often contain germ cells of female morphology rather than male morphology. ovoD1rv23/ovoD1rv23; mle1/mle5 ovaries most often contain germ cells of male morphology rather than female morphology. This phenotype is partially suppressed by SxlM1; ovaries more often contain germ cells of female morphology rather than male morphology. The sterility of ovoM2/ovoM2 and ovoM2/ovoe8K females is partially rescued if they are also carrying SxlM1. The partial sterility of ovoM2/ovoe7E females is rescued if they are also carrying SxlM1.

SxlM1 cannot rescue the XX progeny of females carrying homozygous vir2f germ line clones mated to homozygous vir2f males whether it is paternally or maternally inherited. Does not rescue the lethality of embryos derived from females with homozygous vir3 or vir4 germ line clones mated to vir+ males.

The presence of SxlM1, failed to rescue female lethality in vir transheterozygotes. vir2f/vir- males are fertile in the presence of SxlM1.

Suppresses the dominant female lethality of Sxlf1 and SxlfP7B0 in embryos derived from snfe8H mothers.

When the SxlM1 allele is present on the Df(1)sc19 chromosome the reduction in viability of females that are transheterozygous for Df(1)sc19 and run2 or run3 is suppressed.

The number of vitellogenic eggs produced by ovoD2 heterozygous females is increased by SxlM1.

SxlM1 completely suppresses hhb.PP female lethality and schb.PP male lethality.

Females of the genotype Df(1)HC244, SxlM1/Sxlf1 are fertile and have no male transformations. SxlM1 rescues the zygotic lethal and sex transforming effect of the deficiency: this suggests that snf is involved in the activation of Sxl+ in females. Partial rescue of the maternal effect is seen. Males carrying SxlM1 can survive if they are also mutant for snf. They have several abnormalities: sex combs are a mosaic of male and female bristles, reduced and rotated genitalia, sternite 6 is covered in bristles and sternite 7 is sometimes present.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Has female gene activity even when the normally obligatory level of da+ positive regulatory activity is greatly reduced.

Can partially suppress sexual transformation of germ cells in otu mutant ovaries.

Insertion in SxlM1 does not affect recombination frequency appreciably. Recombination distance between Sxlf9 and SxlM1 is 0.007cM.

Constitutively active Sxl allele.

Constitutive allele.

The roo elements in SxlM1 and SxlM2 have different restriction maps.

Transposon induced constitutive Sxl allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (61)