STUDIES ON THE SEX-SPECIFIC LETHALS OF DROSOPHILA MELANOGASTER. V. SEX TRANSFORMATION CAUSED BY INTERACTIONS BETWEEN A FEMALE-SPECIFIC LETHAL, Sxl  f#1, AND THE MALE-SPECIFIC LETHALS mle(3)132, msl-2  27, AND mle

Genetics ◽  
1982 ◽  
Vol 102 (2) ◽  
pp. 233-243
Author(s):  
T Uenoyama ◽  
A Fukunaga ◽  
K Ioshi
Keyword(s):  
Drosophila Melanogaster ◽  
Morphological Changes ◽  
External Genitalia ◽  
Sexually Dimorphic ◽  
Female Progeny ◽  
Lethal Mutant ◽  
Male Type ◽  
Male Specific Lethal ◽  
Female Specific ◽  
Male Specific

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.

scholarly journals Pleiotropic Roles of the Orthologue of the Drosophila melanogaster Intersex Gene in the Brown Planthopper

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 379
Author(s):  
Hou-Hong Zhang ◽  
Yu-Cheng Xie ◽  
Han-Jing Li ◽  
Ji-Chong Zhuo ◽  
Chuan-Xi Zhang
Keyword(s):  
Drosophila Melanogaster ◽  
Reproductive System ◽  
Splice Variants ◽  
Brown Planthopper ◽  
Nilaparvata Lugens ◽  
Vital Role ◽  
Sexually Dimorphic ◽  
Specific Product ◽  
Reproductive Ability ◽  
Female Specific

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.

scholarly journals Rapid Evolution of Autosomal Binding Sites of the Dosage Compensation Complex in Drosophila melanogaster and Its Association With Transcription Divergence

2021 ◽  
Vol 12 ◽  
Author(s):  
Aimei Dai ◽  
Yushuai Wang ◽  
Anthony Greenberg ◽  
Zhongqi Liufu ◽  
Tian Tang
Keyword(s):  
Drosophila Melanogaster ◽  
Dosage Compensation ◽  
Binding Sites ◽  
Protein Sequence ◽  
Rapid Evolution ◽  
Close Relative ◽  
Sequence Evolution ◽  
Male Specific Lethal ◽  
Msl Complex ◽  
Male Specific

How pleiotropy influences evolution of protein sequence remains unclear. The male-specific lethal (MSL) complex in Drosophila mediates dosage compensation by 2-fold upregulation of the X chromosome in males. Nevertheless, several MSL proteins also bind autosomes and likely perform functions not related to dosage compensation. Here, we study the evolution of MOF, MSL1, and MSL2 biding sites in Drosophila melanogaster and its close relative Drosophila simulans. We found pervasive expansion of the MSL binding sites in D. melanogaster, particularly on autosomes. The majority of these newly-bound regions are unlikely to function in dosage compensation and associated with an increase in expression divergence between D. melanogaster and D. simulans. While dosage-compensation related sites show clear signatures of adaptive evolution, these signatures are even more marked among autosomal regions. Our study points to an intriguing avenue of investigation of pleiotropy as a mechanism promoting rapid protein sequence evolution.

scholarly journals Disparate regulation of imd drives sex differences in infection pathology in Drosophila melanogaster

2020 ◽  
Author(s):  
Crystal M. Vincent ◽  
Marc S. Dionne
Keyword(s):  
Drosophila Melanogaster ◽  
Negative Regulator ◽  
Sexually Dimorphic ◽  
Wild Type ◽  
Functional Importance ◽  
Male And Female ◽  
Immune Activity ◽  
Imd Pathway ◽  
Independent Effects ◽  
Female Specific

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.

scholarly journals STUDIES ON THE SEX-SPECIFIC LETHALS OF DROSOPHILA MELANOGASTER. II. FURTHER STUDIES ON A MALE-SPECIFIC LETHAL GENE, MALELESS

Genetics ◽  
1976 ◽  
Vol 84 (2) ◽  
pp. 257-266
Author(s):  
Atsumi Tanaka ◽  
Akihiro Fukunaga ◽  
Kugao Oishi
Keyword(s):  
Drosophila Melanogaster ◽  
Larval Stage ◽  
Maternal Effect ◽  
Sex Differentiation ◽  
Pupal Stage ◽  
Imaginal Discs ◽  
Lethal Gene ◽  
Male Specific Lethal ◽  
Male Specific

ABSTRACT Effects of a second chromosome male-specific lethal gene, maleless (mle), of Drosophila melanogaster were further studied. It was shown that, although no maternal effect was seen with respect to the male-specific lethality, the lethal stage was influenced by whether parental females were homozygous or heterozygous for mle. Thus, in the former mle/mle males died mostly in the late third instar larval stage, while in the latter practically all males survived to the pupal stage. In the dying mle/mle male pupae complete differentiation of adult external head and thorax structures was often observed but that of abdominal structures was incomplete forming only a few segments in most cases. Imaginal discs from third instar mle/mle male larvae which were produced by mle/mle mothers and were destined to die as larvae were able to differentiate into adult structures upon transplantation into normal third instar larval hosts.—A somewhat elaborated version of the previously presented hypothesis (Fukunaga, Tanaka and Oishi 1975) was discussed as to the possible presence of a class of sex-specific lethals which are not related to the process of primary sex differentiation

scholarly journals TWO CLOSELY LINKED MUTATIONS IN DROSOPHILA MELANOGASTER THAT ARE LETHAL TO OPPOSITE SEXES AND INTERACT WITH DAUGHTERLESS

Genetics ◽  
1978 ◽  
Vol 90 (4) ◽  
pp. 683-697
Author(s):  
Thomas W Cline
Keyword(s):  
Maternal Effect ◽  
Spontaneous Mutation ◽  
Dominant Male ◽  
Lethal Effects ◽  
Male Specific Lethal ◽  
Constitutive Mutation ◽  
Sex Lethal ◽  
The Right ◽  
Female Specific ◽  
Male Specific

ABSTRACT A new spontaneous mutation named Sex-lethal, Male-specific #1 (SxlM1) is described that is lethal to males, even in the presence of an Sxl  + duplication. Females homozygous for SxlM1 are fully viable. This dominant, male-specific lethal mutation is on the X chromosome approximately 0.007 map units to the right of a previously isolated female-specific mutation, Female-lethal, here renamed Sex-lethal, Female-specific #1 (SxlF1). SxlM1 and SxlF1 are opposite in nearly every respect, particularly with regard to their interaction with the maternal effect of the autosomal mutation, daughterless (da). Females that are homozygous for da produce defective eggs that cannot support female (XX) development. A single dose of SxlM1 enables daughters to survive this da female-specific lethal maternal effect. A duplication of the Sxl locus weakly mimics this action of SxlM1. In contrast, SxlF1 and a deficiency for Sxl, strongly enhance the female-lethal effects of da. The actions of SxlM1 and SxlF1 are explained by a model in which expression of the Sxl locus is essential for females, lethal for males, and under the control of a product of the da locus. It is suggested that SxlM1 is a constitutive mutation at the Sxl locus.

scholarly journals Modulation of MSL1 Abundance in Female Drosophila Contributes to the Sex Specificity of Dosage Compensation

Genetics ◽  
1998 ◽  
Vol 150 (2) ◽  
pp. 699-709 ◽  
Author(s):  
Kimberly A Chang ◽  
Mitzi I Kuroda
Keyword(s):  
Dosage Compensation ◽  
Ectopic Expression ◽  
Negative Regulation ◽  
Limiting Factor ◽  
Control Mechanisms ◽  
Linked Gene ◽  
Male Specific Lethal ◽  
Sex Specificity ◽  
Female Specific ◽  
Male Specific

Abstract Dosage compensation in Drosophila is the mechanism by which X-linked gene expression is made equal in males and females. Proper regulation of this process is critical to the survival of both sexes. Males must turn the male-specific lethal (msl)-mediated pathway of dosage compensation on and females must keep it off. The msl2 gene is the primary target of negative regulation in females. Preventing production of MSL2 protein is sufficient to prevent dosage compensation; however, ectopic expression of MSL2 protein in females is not sufficient to induce an insurmountable level of dosage compensation, suggesting that an additional component is limiting in females. A candidate for this limiting factor is MSL1, because the amount of MSL1 protein in females is reduced compared to males. We have identified two levels of negative regulation of msl1 in females. The predominant regulation is at the level of protein stability, while a second regulatory mechanism functions at the level of protein synthesis. Overcoming these control mechanisms by overexpressing both MSL1 and MSL2 in females results in 100% female-specific lethality.

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