Reduction In Wing Size Research Articles

The Effect of Global Warming on Migration of Butterflies

Certainly, global warming is one of the most important environmental problems of mankind today. Increased human activities, especially in the last few decades, like burning fossil fuels, increasing CO2 emissions, deforestation, and other practices have exacerbated the global warming phenomenon. The increase in greenhouse gases leads to an increase in temperatures above the normal rate and this causes fires, droughts, sandstorms, high soil salinity, and fluctuations in precipitation. These changes in the environment affect not only humans but also all living organisms, including insects. Insects are the largest group of living organisms on earth. Therefore, one of the creatures that will be most affected by these changes is insects. Increasing temperatures, rising CO2 levels, and changing rainfall patterns may affect the interaction between plants and insects. For example; the development of insects may accelerate, insect pests and insect-borne diseases, the number of generations in a year and winter survival may increase, the geographical distribution may expand, biological control of the pests may decrease, and as a result of all these, economic losses in crops may increase. Global warming may also affect the migration of insects, in particular, butterflies of which about 600 species have migratory behavior. This may be due to several factors, including the loss of the habitats on which the larvae feed, the nectar resources and the deterioration of their winter habitats, the adaptability and productivity problems in their new habitats, the attack of natural enemies, the disruption of migration signals and the change in wind patterns. In addition, the migration of butterflies may increase with the effect of global warming. Moreover, an increase in temperatures can also cause changes in butterfly morphology, e.g., a reduction in wing size that reduced their flight activity. In this review, we discussed the impact of global warming on butterfly migration.

Drosophila functional screening of de novo variants in autism uncovers damaging variants and facilitates discovery of rare neurodevelopmental diseases.

SUMMARYIndividuals with autism spectrum disorder (ASD) exhibit an increased burden of de novo mutations (DNMs) in a broadening range of genes. While these studies have implicated hundreds of genes in ASD pathogenesis, which DNMs cause functional consequences in vivo remains unclear. We functionally test the effects of ASD missense DNMs using Drosophila through “humanization” rescue and overexpression-based strategies. We examine 79 ASD variants in 74 genes identified in the Simons Simplex Collection and find 38% of them to cause functional alterations. Moreover, we identify GLRA2 as the cause of a spectrum of neurodevelopmental phenotypes beyond ASD in 13 previously undiagnosed subjects. Functional characterization of variants in ASD candidate genes points to conserved neurobiological mechanisms and facilitates gene discovery for rare neurodevelopmental diseases.

MicroRNA miR-7 contributes to the control of Drosophila wing growth.

The control of organ growth is critical for correct animal development. From flies to mammals, the mechanisms regulating growth are conserved and the role of microRNAs in this process is emerging. The conserved miR-7 has been described to control several aspects of development. Here, we have analyzed the function of miR-7 during Drosophila wing development. We found that loss of miR-7 function results in a reduction of wing size and produces wing cells that are smaller than wild type cells. We also found that loss of miR-7 function interferes with the cell cycle by affecting the G1 to S phase transition. Further, we present evidence that miR-7 is expressed in the wing imaginal discs and that the inactivation of miR-7 increases the expression of Cut and Senseless proteins in wing discs. Finally, our results show that the simultaneous inactivation of miR-7 and either cut, Notch, or dacapo rescues miR-7 loss of function wing size reduction phenotype. The results from this work reveal, for the first time, that miR-7 functions to regulate Drosophila wing growth by controlling cell cycle phasing and cell mass through its regulation of the expression of dacapo and the Notch signaling pathway.

Observations on mermithid parasitism (Nematoda: Mermithidae) in two species of Lasius ants (Hymenoptera: Formicidae)

The morphological effects of nematode parasitism by Pheromermis myrmecophila were investigated in two species of ants, Lasius flavus and Lasius niger, collected on Clare Island, Ireland. Infected males and queens were found for L. flavus but only infected queens in L. niger. The numbers of nematodes present in each infected specimen were counted and their lengths were measured. Head width, femur length and wing measurements were made for infected and non-infected individuals of both species. In queens, the length of the nematodes decreased as the number per ant increased. When single nematodes were present their mean lengths were significantly greater in L. flavus than in L. niger. In addition to the reduction in wing size for all parasitized specimens, head widths and femur lengths of the queens were significantly different in both species. A log–log graph of radial cell length versus width suggested a linear reduction of wing size.

Interpretation of the Wingless Gradient Requires Signaling-Induced Self-Inhibition

In a classical view of development, a cell can acquire positional information by reading the local concentration of a morphogen independently of its neighbors. Accordingly, in Drosophila, the morphogen Wingless produced in the wing's prospective distal region activates target genes in a dose-dependent fashion to organize the proximodistal pattern. Here, we show that, in parallel, Wingless triggers two nonautonomous inhibitory programs that play an important role in the establishment of positional information. Cells flanking the source of Wingless produce a negative signal (encoded by notum) that inhibits Wingless signaling in nearby cells. Additionally, in response to Wingless, all prospective wing cells produce an unidentified signal that dampens target gene expression in surrounding cells. Thus, cells influence each other's response to Wingless through at least two modes of lateral inhibition. Without lateral inhibition, some cells acquire ectopic fates. Lateral inhibition may be a general mechanism behind the interpretation of morphogen gradients.

WHAT GROUNDS SOME BIRDS FOR LIFE? MOVEMENT AND DIVING IN THE SEXUALLY DIMORPHIC GALÁPAGOS CORMORANT

Flightlessness in previously volant birds is taxonomically widespread and thought to occur when the costs of having a functional flight apparatus outweigh the benefits. Loss of the ability to fly relaxes body mass constraints which can be particularly advantageous in divers, because underwater performance correlates with mass. The Galápagos CormorantPhalacrocorax harrisiis flightless and the largest of its 27‐member genus. Here, the loss of flight, and consequent reduced foraging range, could be compensated by enhanced dive performance. Over three years, 46 Galápagos Cormorants were successfully equipped with time–depth–temperature recorders, and 30 birds with GPS recorders during the breeding season. Birds foraged at a mean of 690 m from the nest and just 230 m from the nearest coast, confirming an extremely limited foraging range during the breeding season and corresponding increased potential for intraspecific competition. Although the maximum recorded dive depth of 73 m tallied with the species body mass, >90% of dives were conducted in water <15 m deep. The heavier males foraged in different areas and dived longer and deeper than females, which exposed males to colder water. Consideration of how plumage insulation decreases with depth indicates that diving males should lose 30% more heat than females, although this may be partially compensated by their lower surface area : volume ratio. A simple model highlights how energy expenditure from swimming underwater due to buoyancy and energy lost as heat have opposing trends with increasing depth, leading to the prediction of an optimum foraging depth defined by the volume of plumage air and water temperature. This has ramifications for all diving seabirds. It is proposed that the reduction in wing size, together with energy‐expensive flight musculature, allows the Galápagos Cormorant to be more efficient at shallow depths than other seabirds, but only in warm equatorial waters. The high prey density and predictability of benthic prey in defined areas of the Galápagos can be particularly well exploited by this flightless species, with its limited foraging range, but the Galápagos Cormorant is unlikely to be able to accommodate much change in environmental conditions.

Dynamics of in vivo power output and efficiency of Nasonia asynchronous flight muscle

By simultaneously measuring aerodynamic performance, wing kinematics, and metabolic activity, we have estimated the in vivo limits of mechanical power production and efficiency of the asynchronous flight muscle (IFM) in three species of ectoparasitoid wasps genus Nasonia (N. giraulti, N. longicornis, and N. vitripennis). The 0.6 mg animals were flown under tethered flight conditions in a flight simulator that allowed modulation of power production by employing an open-loop visual stimulation technique. At maximum locomotor capacity, flight muscles of Nasonia are capable to sustain 72.2 +/- 18.3 W kg(-1) muscle mechanical power at a chemo-mechanical conversion efficiency of approximately 9.8 +/- 0.9%. Within the working range of the locomotor system, profile power requirement for flight dominates induced power requirement suggesting that the cost to overcome wing drag places the primary limit on overall flight performance. Since inertial power is only approximately 25% of the sum of induced and profile power requirements, Nasonia spp. may not benefit from elastic energy storage during wing deceleration phases. A comparison between wing size-polymorphic males revealed that wing size reduction is accompanied by a decrease in total flight muscle volume, muscle mass-specific mechanical power production, and total flight efficiency. In animals with small wings maximum total flight efficiency is below 0.5%. The aerodynamic and power estimates reported here for Nasonia are comparable to values reported previously for the fruit fly Drosophila flying under similar experimental conditions, while muscle efficiency of the tiny wasp is more at the lower end of values published for various other insects.

RNA interference from a CAX trinucleotide repeat.

The use of RNA interference (RNAi) techniques, combined with a spatially controlled expression of doublestranded RNA (dsRNA), provides a convenient method for producing cell-type-specific perturbations of gene function (Fortier and Belote, 2000; Martinek et al., 2000). While studying the function of the Drosophila miniature-dusky (m-dy) gene complex (DiBartolomeis et al., 2002), we produced transgenic flies expressing a dsRNA that would permit silencing of the dy gene (P{UAS-dy-dsRNA}; Fig. 1a). The m and dy genes share sequence similarity and both encode fly Cuticulin proteins (DiBartolomeis et al., 2002) that are required at the pupal stage of development (Newby and Jackson, 1995) for normal wing differentiation. In the absence of m-dy products, the wing is reduced in size, due to an autonomous effect on the size and/or shape of wing epidermal cells (Newby et al., 1991). Although a reduction in wing size is the only obvious morphological phenotype in m-dy flies, certain mutants exhibit reduced viability and/or fertility (Newby et al., 1991). To examine the phenotypic effects of the UAS-dy-dsRNA transgene, we ectopically expressed it within wing tissues, taking advantage of four different existing Drosophila GAL4 driver strains: P{GawB}30A, P{GawB}34B, MS1096, and A9. The first two strains are described in Flybase, the last two were obtained from M. O’Connor (Univ. of Minnesota). All four strains provide expression in wing and other imaginal discs. Previously characterized dy mutants have small wings of normal proportion ( 2/3 of the wild-type size), whereas m mutants show a more extreme reduction in wing size and the wings are malproportioned compared to the wild type. The relatively less severe phenotype of dy mutants approximates the null phenotype for this gene, as dy/dy and dy/Df flies exhibit similar wing defects (Newby et al., 1991). Expression of UAS-dy-dsRNA with three out of four of the GAL4 drivers (P{GawB}34B, MS1096, and A9) was associated with a wing phenotype, the severity of which was dependent on the particular driver (Table 1). The fourth driver, P{GawB}30A, caused complete lethality at the late pupal stage (Table 1) and pharate adults were not dissected for examination. We were surprised that ectopic expression of UAS-dydsRNA, using either MS1096 or A9 as a driver, produced a wing phenotype more severe than that observed in existing single dy or m mutants (Table 1; Fig. 1; data not shown). Both of these GAL4 transgenes are known to drive expression in the developing wings, although MS1096 has a slightly broader pattern of expression (M. O’Connor, pers. commun.) that might explain the more severe wing phenotype compared to A9. A wing phenotype was observed with these two drivers using three independent UAS-dy-dsRNA insertions (19-4, 28-1, and 38-1), so the phenotype is not a consequence of transgene insertion. In addition, wing abnormalities were not observed in control siblings carrying any one of the GAL4 drivers or the UAS-dy-dsRNA transgene alone (not shown). Interestingly, the size of the wing in MS1096 or A9; UAS-dy-dsRNA flies is similar to that of a m-dy double mutant called Df(1)m (Fig. 1f), which is known to carry a chromosomal deletion removing only m and dy (Roberts and Jackson, 1997). Given the known sequence similarity between m and dy, such a result suggests that the UAS-dy-dsRNA transgene might target both m and dy RNAs for destruction (see below). Other abnormalities, in addition to wing phenotypes, were observed in our GAL4/UAS-dy-dsRNA crosses. Lethality was observed in populations carrying UAS-dydsRNA with any of the four GAL4 transgenes (Table 1) and the degree of lethality was dependent on the GAL4 driver (see Table 1 notes). In many crosses, much of this lethality appeared to occur at the late pupal stage, although we cannot exclude death at earlier developmental stages. As indicated, the combination of P{GawB}30A and UAS-dy-dsRNA was completely lethal, whereas the other drivers were semilethal in combination with the UAS transgene. Some of this observed lethality is attributable to elimination of m-dy function(s), as Df(1)m also exhibits poor viability (Roberts and Jackson, 1997). Although the general morphology of surviving GAL4; UAS-dy-dsRNA flies is relatively normal, and females are fertile (not shown), these flies nonetheless exhibit additional phenotypes that might reflect targeting of genes other than m and dy. A comparison of m and GAL4; UAS-dy-dsRNA flies, for example, indicates that the mor-

The translational inhibitor 4E-BP is an effector of PI(3)K/Akt signalling and cell growth in Drosophila.

The initiation factor 4E for eukaryotic translation (eIF4E) binds the messenger RNA 5'-cap structure and is important in the regulation of protein synthesis. Mammalian eIF4E activity is inhibited when the initiation factor binds to the translational repressors, the 4E-binding proteins (4E-BPS). Here we show that the Drosophila melanogaster 4E-BP (d4E-BP) is a downstream target of the phosphatidylinositol-3-OH kinase (PI(3)K) signal-transduction cascade, which affects the interaction of d4E-BP with eIF4E. Ectopic expression of a highly active d4E-BP mutant in wing-imaginal discs causes a reduction of wing size, brought about by a decrease in cell size and number. A marked reduction in cell size was also observed in post-mitotic cells. Expression of d4E-BP in the eye and wing together with PI(3)K or dAkt1, the serine/threonine kinase downstream of PI(3)K, resulted in suppression of the growth phenotype elicited by these kinases. Our results support a role for d4E-BP as an effector of cell growth.