SummarySex determination offers an opportunity to address many classic questions of developmental biology. In addition, because sex determination evolves rapidly, it offers an opportunity to investigate the evolution of genetic hierarchies. Sex determination in Drosophila melanogaster is controlled by the master regulatory gene, Sex lethal (Sxl ). DmSxl controls the alternative splicing of a downstream gene, transformer (tra), which acts with tra2 to control alternative splicing of doublesex (dsx). DmSxl also controls its own splicing, creating an autoregulatory feedback loop that ensures expression of Sxl in females, but not males. A recent paper (1) has shown that in the dipteran Ceratitis capitata later (downstream) steps in the regulatory hierarchy are conserved, while earlier (upstream) steps are not. Cctra is regulated by alternative splicing and apparently controls the alternative splicing of Ccdsx. However, Cctra is not regulated by CcSxl. Instead it appears to autoregulate in a manner similar to the autoregulation seen with DmSxl.

In many animal species, learning and memory have been found to play important roles in regulating intra-and interspecific behavioral interactions in varying environments. In such contexts, aggression is commonly used to obtain desired resources. Previous defeats or victories during aggressive interactions have been shown to influence the outcome of later contests, revealing loser and winner effects. In this study, we asked whether short-and/or long-term behavioral consequences accompany victories and defeats in dyadic pairings between male Drosophila melanogaster and how long those effects remain. The results demonstrated that single fights induced important behavioral changes in both combatants and resulted in the formation of short-term loser and winner effects. These decayed over several hours, with the duration depending on the level of familiarity of the opponents. Repeated defeats induced a long-lasting loser effect that was dependent on de novo protein synthesis, whereas repeated victories had no long-term behavioral consequences. This suggests that separate mechanisms govern the formation of loser and winner effects. These studies aim to lay a foundation for future investigations exploring the molecular mechanisms and circuitry underlying the nervous system changes induced by winning and losing bouts during agonistic encounters.loser/winner effects | aggression | learning and memory | behavior | Drosophila melanogaster

Genes and prior experience both influence the behavior of animals, but the relative contribution of each to fighting behavior in Drosophila remains unclear. To address this issue, we bred hyperaggressive flies by selecting winners of fights over 34-37 generations. Males of this strain initiate fights sooner, retaliate more often, and regularly defeat opponents from the nonselected parent Canton-S strain. After a defeat, however, these highly aggressive flies lose their second fights against socially naïve counterparts. Defeated flies also lunge and retaliate less after experiencing a loss, suggesting that the subsequent losses result from flies becoming less aggressive. Remarkably, flies that were once capable of engaging in highintensity boxing and tussling patterns of behavior for extended periods of time often do not even engage in mid-intensity lunging after a single defeat. Furthermore, these formerly highly aggressive flies lose all competitive advantage over nonselected Canton-S after experiencing a loss. Lastly, females were more likely to copulate with males from the nonselected parent line than with the hyperaggressive strain.behavior | fighting | flies | learning | memory

fl(2)d, the Drosophila homolog of Wilms'-tumor-1-associated protein (WTAP), regulates the alternative splicing of Sex-lethal (Sxl), transformer (tra), and Ultrabithorax (Ubx). Although WTAP has been found in functional human spliceosomes, exactly how it contributes to the splicing process remains unknown. Here we attempt to identify factors that interact genetically and physically with fl(2)d. We begin by analyzing the Sxl-Fl(2)d protein-protein interaction in detail and present evidence suggesting that the female-specific fl(2)d 1 allele is antimorphic with respect to the process of sex determination. Next we show that fl(2)d interacts genetically with early acting general splicing regulators and that Fl(2)d is present in immunoprecipitable complexes with Snf, U2AF50, U2AF38, and U1-70K. By contrast, we could not detect Fl(2)d complexes containing the U5 snRNP protein U5-40K or with a protein that associates with the activated B spliceosomal complex SKIP. Significantly, the genetic and molecular interactions observed for Sxl are quite similar to those detected for fl(2)d. Taken together, our findings suggest that Sxl and fl(2)d function to alter splice-site selection at an early step in spliceosome assembly. I N Drosophila melanogaster, sexual identity is initially determined by the X chromosome-to-autosome (A) ratio (Cline and Meyer 1996). The system that measures the X-to-A ratio turns on the Sex-lethal (Sxl) gene in female (XX) embryos by activating the Sxl establishment promoter, Sxl-Pe. In males (XY), this promoter is not activated and Sxl remains off. The establishment promoter is active for only a brief period in precellular blastoderm female embryos, and maintaining Sxl in the on state during the remainder of development in females depends upon an autoregulatory mechanism in which Sxl proteins direct their own synthesis by promoting the female-specific splicing of Sxl pre-mRNAs transcribed from the Sxl maintenance promoter (SxlPm). In this autoregulatory loop, Sxl proteins bind to multiple sites in the large introns located upstream and downstream of the male-specific third exon and promote the joining of the 59 splice site of exon 2 to the 39 splice site of exon 4, skipping exon 3. The translation of the resulting Sxl mRNA ensures the maintenance of female identity by providing a continuous source of Sxl protein. In males, the third exon is incorporated into the Sxl mRNA by the default splicing machinery. The male-specific exon has several in-frame stop codons that prematurely truncate the Sxl open reading frame, which begins in exon 2, resulting in the production of a truncated, nonfunctional polypeptide. Sxl controls the majority of female development by regulating the female-specific splicing of transformer (tra) pre-mRNA. This female-specific Tra protein (Tra F ) then regulates the alternative splicing of the transcription factors doublesex and fruitless. In addition, Sxl expression is required for female viability because it turns off the gene msl-2. MSL-2 is a component of the male-speci...