scholarly journals A genetic analysis of intersex, a gene regulating sexual differentiation in Drosophila melanogaster females.

Genetics ◽  
1995 ◽  
Vol 139 (4) ◽  
pp. 1649-1661 ◽  
Author(s):  
B A Chase ◽  
B S Baker

Abstract Sex-type in Drosophila melanogaster is controlled by a hierarchically acting set of regulatory genes. At the terminus of this hierarchy lie those regulatory genes responsible for implementing sexual differentiation: genes that control the activity of target loci whose products give rise to sexually dimorphic phenotypes. The genetic analysis of the intersex (ix) gene presented here demonstrates that ix is such a terminally positioned regulatory locus. The ix locus has been localized to the cytogenetic interval between 47E3-6 and 47F11-18. A comparison of the morphological and behavioral phenotypes of homozygotes and hemizygotes for three point mutations at ix indicates that the null phenotype of ix is to transform diplo-X animals into intersexes while leaving haplo-X animals unaffected. Analysis of X-ray induced, mitotic recombination clones lacking ix+ function in the abdomen of diplo-X individuals indicates that the ix+ product functions in a cell-autonomous manner and that it is required at least until the termination of cell division in this tissue. Taken together with previous analyses, our results indicate that the ix+ product is required to function with the female-specific product of doublesex to implement appropriate female sexual differentiation in diplo-X animals.

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 379
Author(s):  
Hou-Hong Zhang ◽  
Yu-Cheng Xie ◽  
Han-Jing Li ◽  
Ji-Chong Zhuo ◽  
Chuan-Xi Zhang

Intersex(ix), a gene involved in the sex-determining cascade of Drosophila melanogaster, works in concert with the female-specific product of doublesex (dsx) at the end of the hierarchy to implement the sex-specific differentiation of sexually dimorphic characters in female individuals. In this study, the ix homolog was identified in the brown planthopper (BPH), Nilaparvata lugens, which contained two splice variants expressed in both female and male insects. We found that Nlix played a vital role in the early nymphal development of BPH, showing an accumulated effect. RNAi-mediated knockdown of Nlix at 4th instar led to the external genital defects in both sexes, consequently resulting in the loss of reproductive ability in female and male individuals. After dsRNA injection, the males were normal on testes, while the females had defective ovarian development. Nlix was also required for early embryogenesis. Notably, when the dsNlix microinjection was performed in newly emerged females, the copulatory bursas were abnormally enlarged while the other tissues of the reproductive system developed normally. Our results demonstrated the pleiotropic roles of Nlix in embryogenesis and development of the reproductive system in a hemimetabolous insect species.


Genetics ◽  
1994 ◽  
Vol 136 (1) ◽  
pp. 195-207
Author(s):  
M A Pultz ◽  
G S Carson ◽  
B S Baker

Abstract Sex determination in Drosophila is controlled by a cascade of regulatory genes. Here we describe hermaphrodite (her), a new component of this regulatory cascade with pleiotropic zygotic and maternal functions. Zygotically, her+ function is required for female sexual differentiation: when zygotic her+ function is lacking, females are transformed to intersexes. Zygotic her+ function may also play a role in male sexual differentiation. Maternally, her+ function is needed to ensure the viability of female progeny: a partial loss of her+ function preferentially kills daughters. In addition, her has both zygotic and maternal functions required for viability in both sexes. Temperature sensitivity prevails for all known her alleles and for all of the her phenotypes described above, suggesting that her may participate in an intrinsically temperature-sensitive process. This analysis of four her alleles also indicates that the zygotic and maternal components of of her function are differentially mutable. We have localized her cytologically to 36A3-36A11.


1988 ◽  
Vol 89 (1) ◽  
pp. 39-47 ◽  
Author(s):  
C. Gonzalez ◽  
J. Casal ◽  
P. Ripoll

Mutation in the gene merry-go-round (mgr) of Drosophila causes a variety of phenotypic traits in somatic and germinal tissues, such as polyploid cells, metaphasic arrest, postmeiotic cysts with 16 nuclei, and spermatids with four times the normal chromosome content. The most characteristic phenotype is the appearance of mitotic and meiotic figures where all chromosomes are arranged in a circle. Treatment with anti-mitotic drugs and the phenotype of double mutants mgr asp (asp being a mutation altering the spindle) show that these circular figures need a functional spindle for their formation. These abnormal figures are caused by monopolar spindles similar to those observed after different treatments in several organisms. All mutant traits indicate that mgr performs a function necessary for the correct behaviour of centrosomes, thus opening this organelle to genetic analysis.


1984 ◽  
Vol 44 (2) ◽  
pp. 125-132 ◽  
Author(s):  
James A. Birchler

SUMMARYA modifier locus is described that alters the level of phenotypic expression of the third chromosome mutant glass in a sex specific manner. Alternative alleles either confer a sexually dimorphic level of pigment in glass mutants, with the male being greater, or cause similar expression in the two sexes. The alleles are indistinguishable in females but produce the respective phenotypes in males. The gene maps to the tip of the X chromosome at position 0·96 ± 0·11. Cytologically, the locus is present between polytene bands 3A6–8 and 3C2–3 as determined by its inclusion in translocated X segments in w + Y, Dp(l;2)w70h31 and Dp(l;3)w67k27 The dimorphic allele is dominant to the nondimorphic condition in males heterozygous for an insertional translocation carrying the dimorphic allele and a normal chromosome carrying the nondimorphic form. The dimorphic allele in two doses in males does not exhibit a dosage effect. The modifier phenotype is unaffected in two X flies by the presence of the transformer mutation.


2020 ◽  
Author(s):  
Crystal M. Vincent ◽  
Marc S. Dionne

AbstractMale and female animals exhibit differences in infection outcomes. One possible source of sexually dimorphic immunity is sex-specific costs of immune activity or pathology, but little is known about the independent effects of immune-induced versus microbe-induced pathology, and whether these may differ for the sexes. Here, through measuring metabolic and physiological outputs in wild-type and immune-compromised Drosophila melanogaster, we test whether the sexes are differentially impacted by these various sources of pathology and identify a critical regulator of this difference. We find that the sexes exhibit differential immune activity but similar bacteria-derived metabolic pathology. We show that female-specific immune-inducible expression of PGRP-LB, a negative regulator of the Imd pathway, enables females to reduce immune activity in response to reductions in bacterial numbers. In the absence of PGRP-LB, females are more resistant of infection, confirming the functional importance of this regulation and suggesting that female-biased immune restriction comes at a cost.


2002 ◽  
Vol 80 (1) ◽  
pp. 7-14 ◽  
Author(s):  
M. ACHARYYA ◽  
R. N. CHATTERJEE

An allele of intersex (ix5) of Drosophila melanogaster has been characterized. The genetic analysis of the allele demonstrated that like other point mutations of ix, the ix5 allele also transformed diplo-X individuals into intersexes. The ix5 mutation also affects the arrangement of sex comb bristles on the forelegs of males, although they had morphologically nearly normal male genitalia. They often fail to display a sustained pattern of courtship activity when tested. Orcein-stained squash preparations of testes from ix5 males revealed a defect in spermatogenesis. Our results, taken together with those of McRobert & Tompkins (1985), indicate that the ix+ gene also functions in male sex determination.


Genetics ◽  
1982 ◽  
Vol 102 (2) ◽  
pp. 233-243
Author(s):  
T Uenoyama ◽  
A Fukunaga ◽  
K Ioshi

ABSTRACT Interactions between a female-specific lethal mutant, Sxlf  #1, and each of three male-specific lethal mutants, mle(3)132, msl-2  27 and mle, of Drosophila melanogaster were observed to produce morphological changes in various sexually dimorphic external characters. Chromosomal females heterozygous for Sxlf  #1 and homozygous for any one of the male-specific lethals (and to a lesser degree heterozygous for male-specific lethals) sometimes had sex combs, male-type tergites, male-type sternites, male-type anal plates or male-type external genitalia. Penetrance was not high and expression was often incomplete; single individuals never had all the sexually dimorphic structures transformed. When mothers were homozygous for male-specific lethals, higher proportions of female progeny were affected than when mothers were heterozygous, suggesting a maternal effect.


Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 638-645 ◽  
Author(s):  
B. S. Baker ◽  
K. Burtis ◽  
T. Goralski ◽  
W. Mattox ◽  
R. Nagoshi

The molecular analyses of three of the regulatory genes (transformer (tra), doublesex (dsx), and transformer-2 (tra-2)) controlling sexual differentiation in Drosophila have demonstrated that the control of RNA processing has a major role in regulating somatic sexual differentiation. The activities of both the tra and dsx genes are controlled at the level of RNA processing. In the case of tra the use of different splice acceptor sites results in a functional transcript being produced only in females, whereas at dsx the use of different splice acceptor sites in the two sexes results in the production of transcripts that encode different proteins in males and females. The tra-2 gene has been shown to be necessary for the processing of the dsx pre-mRNA in females and the conceptual translation of a tra-2 cDNA shows that it encodes a protein with similarity to a family of RNA-binding proteins which includes known splicesome components. We previously suggested that the pattern of sexual differentiation and dosage compensation characteristic of a male was a default regulatory state. The findings reviewed here provide a molecular basis for this default expression in males as well as an insight into how females differ from males in control of the expression of these genes. For both the tra and dsx genes the molecular basis of their male (default) state of expression appears to be the processing of their transcripts by the housekeeping RNA splicing machinery. In females the specification of the alternative pattern of splicing at both tra and dsx is by the sex determination regulatory genes that function upstream of them in this regulatory cascade. It seems likely that the activities of these sex determination regulatory genes in females do not provide all of the information that is necessary for proper splicing of the transcripts of the genes downstream of them. Rather we imagine that the products of the Sxl, tra, and tra-2 genes are acting to impose a specificity on the basic cellular splicing machinery.Key words: Drosophila melanogaster, sex determination, sexual differentiation.


Development ◽  
1975 ◽  
Vol 34 (1) ◽  
pp. 19-31
Author(s):  
Gines Morata

Contrabithorax, a mutant of the bithorax system in Drosophila melanogaster produces a partial homeotic transformation of mesothorax (wing) into metathorax (haltere). The wing of a fly homozygous or heterozygous for the mutant is a mosaic of wing and haltere structures. A genetic analysis of the mutant suggests that its phenotype is due to some form of derepression in the wing of two other genes of the bithorax system (bithorax and postbithorax) which are not normally active there. This repression is not complete. The activity of the two genes is below the normal level resulting in only a partial transformation of wing into haltere. Clones of marked cells were generated by X-rays and were found to include both transformed (haltere) and untransformed (wing) territory; this was true even for those generated late in development. Thus the final expression of a cell depends not on its immediate ancestry but perhaps on the level of the products of the wild-type alleles of bithorax and postbithorax.


2021 ◽  
Vol 118 (32) ◽  
pp. e2026554118
Author(s):  
Crystal M. Vincent ◽  
Marc S. Dionne

Male and female animals exhibit differences in infection outcomes. One possible source of sexually dimorphic immunity is the sex-specific costs of immune activity or pathology, but little is known about the independent effects of immune- versus microbe-induced pathology and whether these may differ for the sexes. Here, by measuring metabolic and physiological outputs in Drosophila melanogaster with wild-type and mutant immune responses, we test whether the sexes are differentially impacted by these various sources of pathology and identify a critical regulator of this difference. We find that the sexes exhibit differential immune activity but similar bacteria-derived metabolic pathology. We show that female-specific immune-inducible expression of PGRP-LB, a negative regulator of the immune deficiency (IMD) pathway, enables females to reduce immune activity in response to reductions in bacterial numbers. In the absence of PGRP-LB, females are more resistant to infection, confirming the functional importance of this regulation and suggesting that female-biased immune restriction comes at a cost.


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