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

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.

Genetics ◽  
1976 ◽  
Vol 84 (2) ◽  
pp. 257-266
Author(s):  
Atsumi Tanaka ◽  
Akihiro Fukunaga ◽  
Kugao Oishi

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


Development ◽  
1995 ◽  
Vol 121 (10) ◽  
pp. 3245-3258 ◽  
Author(s):  
G.J. Bashaw ◽  
B.S. Baker

In Drosophila dosage compensation increases the rate of transcription of the male's X chromosome and depends on four autosomal male-specific lethal genes. We have cloned the msl-2 gene and shown that MSL-2 protein is co-localized with the other three MSL proteins at hundreds of sites along the male polytene X chromosome and that this binding requires the other three MSL proteins. msl-2 encodes a protein with a putative DNA-binding domain: the RING finger. MSL-2 protein is not produced in females and sequences in both the 5′ and 3′ UTRs are important for this sex-specific regulation. Furthermore, msl-2 pre-mRNA is alternatively spliced in a Sex-lethal-dependent fashion in its 5′ UTR.


1984 ◽  
Vol 43 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Craig S. Tepper ◽  
Anne L. Terry ◽  
James E. Holmes ◽  
Rollin C. Richmond

SUMMARYThe esterase 6 (Est-6) locus in Drosophila melanogaster is located on the third chromosome and is the structural gene for a carboxylesterase (E.C.3.1.1.1) and is polymorphic for two major electromorphs (slow and fast). Isogenic lines containing X chromosomes extracted from natural populations and substituted into a common genetic background were used to detect unlinked factors that affect the activity of the Est-6 locus. Twofold activity differences of esterase 6 (EST 6) were found among males from these derived lines, which differ only in their X chromosome. These unlinked activity modifiers identify possible regulatory elements. Immunoelectrophoresis was used to estimate quantitatively the levels of specific cross-reacting material in the derived lines. The results show that the variation in activity is due to differences in the amount of EST 6 present. The data are consistent with the hypothesis that there is at least one locus on the X chromosome that regulates the synthesis of EST 6 and that this regulatory locus may be polymorphic in natural populations.


Genetics ◽  
2004 ◽  
Vol 166 (4) ◽  
pp. 1825-1832 ◽  
Author(s):  
Barbara P Rattner ◽  
Victoria H Meller

Abstract The MSL complex of Drosophila upregulates transcription of the male X chromosome, equalizing male and female X-linked gene expression. Five male-specific lethal proteins and at least one of the two noncoding roX RNAs are essential for this process. The roX RNAs are required for the localization of MSL complexes to the X chromosome. Although the mechanisms directing targeting remain speculative, the ratio of MSL protein to roX RNA influences localization of the complex. We examine the transcriptional regulation of the roX genes and show that MSL2 controls male-specific roX expression in the absence of any other MSL protein. We propose that this mechanism maintains a stable MSL/roX ratio that is favorable for localization of the complex to the X chromosome.


2021 ◽  
Vol 12 ◽  
Author(s):  
Aimei Dai ◽  
Yushuai Wang ◽  
Anthony Greenberg ◽  
Zhongqi Liufu ◽  
Tian Tang

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.


Genetics ◽  
1988 ◽  
Vol 118 (2) ◽  
pp. 247-259
Author(s):  
I Kiss ◽  
A H Beaton ◽  
J Tardiff ◽  
D Fristrom ◽  
J W Fristrom

Abstract The 2B5 region on the X chromosome of Drosophila melanogaster forms an early ecdysone puff at the end of the third larval instar. The region contains a complex genetic locus, the Broad-Complex (BR-C) composed of four groups of fully complementing (br, rbp, l(1)2Bc, and l(1)2Bd) alleles, and classes of noncomplementing (npr 1) and partially noncomplementing l(1)2Bab alleles. BR-C mutants prevent metamorphosis, including the morphogenesis of imaginal discs. Results are presented that indicate that the BR-C contains two major functional domains. One, the br domain is primarily, if not exclusively, involved in the elongation and eversion of appendages by imaginal discs. The second, the l(1)2Bc domain, is primarily involved in the fusion of discs to form a continuous adult epidermis. Nonetheless, the two domains may encode products with related functions because in some situations mutants in both domains appear to affect similar developmental processes.


Genetics ◽  
1980 ◽  
Vol 96 (1) ◽  
pp. 165-186 ◽  
Author(s):  
John M Belote ◽  
John C Lucchesi

ABSTRACT A total of 7,416 ethyl methanesulfonate (EMS)-treated second chromosomes and 6,212 EMS-treated third chromosomes were screened for sex-specific lethals. Four new recessive male-specific lethal mutations were recovered. When in homozygous condition, each of these mutations kills males during the late larval or early pupal stages, but has no detectable effect in females. One mutant, mlets, is a temperature sensitive allele of maleless, mle (Fukunaga, Tanaka and Oishi 1975), while the other three mutants identify two new loci: male-specific lethal-1 (msl-1) (two alleles) at map position 2-53.3 and male-specific lethal-2 (msl-2) at 2-9.0.——The male-specific lethality associated with these mutants is not related to the sex per se of the mutant flies, since sex-transforming genes fail to interact with these mutations. Moreover, the presence or absence of a Y chromosome in males or females has no influence on the male-specific lethal action of these mutations. Finally, no single region of the X chromosome, when present as a duplication, is sufficient to rescue males from the lethal effects of msl-1 or msl-2. These results suggest that the number of complete X chromosomes determines whether a fly homozygous for a male-specific lethal mutation lives or dies.


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