roo insertion near the sex-specific exon.
Insertion of a roo element.
partially constitutive due to roo insert near male-specific exon roo insertion
SxlM1,fPw+c suppresses the dominant male-specific lethality of SxlM1.
SxlM1,fΔ33 suppresses the dominant male-specific lethality of SxlM1.
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).
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.
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.
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.
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 | partially of female sterile phenotype of ovoe8K/ovoM2
SxlM1 is a suppressor of lethal | female | larval stage phenotype of virunspecified/vir2f
SxlM1 is a suppressor of female sterile phenotype of otu11
SxlM1 is a suppressor of decreased fecundity | dominant | female phenotype of ovoD2
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 otu10
SxlM1 is a non-suppressor of female sterile phenotype of otu13
SxlM1 is a non-suppressor of female sterile phenotype of otu2
SxlM1, ovoM2/ovoe7E has female semi-sterile phenotype
SxlM1, ovoM2/ovoe7E has female fertile phenotype
SxlM1, otu11/otu13 has female fertile phenotype
SxlM1, otu11 has female fertile phenotype
Df(1)HC244, SxlM1/Sxlf1 has viable phenotype
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.
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.
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.
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.