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

MALELESS, A RECESSIVE AUTOSOMAL MUTANT OF DROSOPHILA MELANOGASTER THAT SPECIFICALLY KILLS MALE ZYGOTES

Genetics ◽  
1975 ◽  
Vol 81 (1) ◽  
pp. 135-141
Author(s):  
Akihiro Fukunaga ◽  
Atsumi Tanaka ◽  
Kugao Oishi
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Larval Stage ◽  
Lethal Gene ◽  
Homozygous Condition ◽  
The Third ◽  
Male Specific Lethal ◽  
Male Specific ◽  
Transforming Genes

ABSTRACT A second chromosome male-specific lethal gene, maleless (mle), in D. melanogaster is described. It kills males but not females in homozygous condition, regardless of whether female parents are heterozygous or homozygous for mle. Many, if not most, homozygous males survive up to the third instar larval stage, but cannot pupate and die eventually as larvae. No interactions with sex-transforming genes, tra and dsx, were observed. It is proposed that mle interacts with a gene(s) on the X chromosome, which is not dosage compensated.

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 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.

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 Drosophila Male-Specific Lethal-4 Protein: Structure/Function Analysis and Dependence on MSL-1 for Chromosome Association

Genetics ◽  
1997 ◽  
Vol 147 (4) ◽  
pp. 1743-1753 ◽  
Author(s):  
Laura M Lyman ◽  
Kyle Copps ◽  
Luca Rastelli ◽  
Richard L Kelly ◽  
Mitzi I Kuroda
Keyword(s):  
Drosophila Melanogaster ◽  
Function Analysis ◽  
Ring Finger ◽  
Loss Of Function ◽  
Stringent Requirement ◽  
Ring Finger Domain ◽  
Male Specific Lethal ◽  
Sitedirected Mutagenesis ◽  
Regulatory Complex ◽  
Male Specific

Abstract MSL-2 is required for the male-specific assembly of a dosage compensation regulatory complex on the X chromosome of Drosophila melanogaster. We found that MSL-2 binds in a reproducible, partial pattern to the male Xchromosome in the absence of MLE or MSL-3, or when ectopically expressed at a low level in females. Moreover, the pattern of MSL-2 binding corresponds precisely in each case to that of MSL-1, suggesting that the two proteins function together to associate with the X. Consistent with this hypothesis, we isolated EMSinduced loss of function msl-1 and msl-2 alleles in a screen for suppressors of the toxic effects of MSL-2 expression in females. We also used sitedirected mutagenesis to determine the importance of the MSL-2 RING finger domain and second cysteine-rich motif. The mutations, including those in conserved zinc coordinating cysteines, confirm that the RING finger is essential for MSL-2 function, while suggesting a less stringent requirement for an intact second motif.

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