Sex-Specific Weight Loss Mediates Sexual Size Dimorphism in Drosophila melanogaster

Testa, Nicholas D.; Ghosh, Shampa M.; Shingleton, Alexander W.

doi:10.1371/journal.pone.0058936

Cited by 82 publications

(127 citation statements)

References 41 publications

(39 reference statements)

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“…The hypoallometric pattern for SSD and isometric pattern for SDtD are thus qualitatively inconsistent, and therefore the sex differences, as well as the SSD allometry not following Rensch's rule displayed in Figure 2, are only distinct for wing size (and not developmental time), which is also true across Drosophila species (Blanckenhorn et al, 2007a). Overall, therefore, sex differences in developmental time cannot explain sex differences in body size, and SDtD cannot explain the allometric pattern of SSD in any simple way, confirming similar conclusions of previous studies (Blanckenhorn et al, 2007a;Testa et al, 2013). Contrary to expectation, we here also found a significant negative genetic correlation between wing size and developmental time that was equal for both sexes (Figure 3).…”

Section: Discussionsupporting

confidence: 85%

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Effect of genomic deficiencies on sexual size dimorphism through modification of developmental time in Drosophila melanogaster

Takahashi

Blanckenhorn

2015

Heredity

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Sexual size dimorphism (SSD), a difference in body size between sexes, is common in many taxa. In insects, females are larger than males in 470% of all taxa in most orders. The fruit fly, Drosophila melanogaster is one prominent model organism to investigate SSD since its clear and representative female-biased SSD and its growth regulation are well studied. Elucidating the number and nature of genetic elements that can potentially influence SSD would be helpful in understanding the evolutionary potential of SSD. Here, we investigated the SSD pattern caused by artificially introduced genetic variation in D. melanogaster, and examined whether variation in SSD was mediated by the sex-specific modification of developmental time. To map the genomic regions that had effects on sexual wing size and/or developmental time differences (SDtD), we reanalyzed previously published genome-wide deficiency mapping data to evaluate the effects of 376 isogenic deficiencies covering a total of~67% of the genomic regions of the second and third chromosomes of D. melanogaster. We found genetic variation in SSD and SDtD generated by genomic deficiencies, and a negative genetic correlation between size and development time. We also found SSD and SDtD allometries that are not qualitatively congruent, which however overall at best only partly help in explaining the patterns found. We identified several genomic deficiencies with the tendency to either exaggerate or suppress SSD, in agreement with quantitative genetic null expectations of many loci with small effects. These novel findings contribute to a better understanding of the evolutionary potential of sexual dimorphism.

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Section: Discussionsupporting

confidence: 85%

“…Testa et al (2013) described complete growth profiles of D. melanogaster males and females, and identified sex-specific growth factors responsible for SSD. They found that growth rate and critical size for pupation significantly contributed to SSD, while developmental time did not.…”

Section: Introductionmentioning

confidence: 99%

Effect of genomic deficiencies on sexual size dimorphism through modification of developmental time in Drosophila melanogaster

Takahashi

Blanckenhorn

2015

Heredity

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“…For the measurement of larval growth trajectories at 258C, female larvae also carried a ubi-GFP transgene (Bloomington Stock Center, 1681) that had been backcrossed into SAM for five generations. This allowed us to conduct experiments exploring the developmental regulation of sexual size dimorphism, described elsewhere [36]. All experiments were conducted at constantlight regime, and fly cultures were maintained at low density (50-60 larvae per 6 ml food) on standard cornmeal -molasses medium.…”

Section: Methods (A) Fly Stocks and Rearingmentioning

confidence: 99%

Temperature-size rule is mediated by thermal plasticity of critical size inDrosophila melanogaster

2013

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Most ectotherms show an inverse relationship between developmental temperature and body size, a phenomenon known as the temperature-size rule (TSR). Several competing hypotheses have been proposed to explain its occurrence. According to one set of views, the TSR results from inevitable biophysical effects of temperature on the rates of growth and differentiation, whereas other views suggest the TSR is an adaptation that can be achieved by a diversity of mechanisms in different taxa. Our data reveal that the fruitfly, Drosophila melanogaster, obeys the TSR using a novel mechanism: reduction in critical size at higher temperatures. In holometabolous insects, attainment of critical size initiates the hormonal cascade that terminates growth, and hence, Drosophila larvae appear to instigate the signal to stop growth at a smaller size at higher temperatures. This is in contrast to findings from another holometabolous insect, Manduca sexta, in which the TSR results from the effect of temperature on the rate and duration of growth. This contrast suggests that there is no single mechanism that accounts for the TSR. Instead, the TSR appears to be an adaptation that is achieved at a proximate level through different mechanisms in different taxa.

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“…1A shows that ablation of the CA had no effect on critical weight. We used the breakpoint method to assay critical weight in CAX and control larvae (15,(20)(21)(22). This method exploits the fact that the relationship between larval weight at starvation and time to pupariation (TTP) changes at critical weight (Fig.…”

Section: Significancementioning

confidence: 99%

Juvenile hormone regulates body size and perturbs insulin signaling in Drosophila

Mirth

Tang

Makohon-Moore

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The role of juvenile hormone (JH) in regulating the timing and nature of insect molts is well-established. Increasing evidence suggests that JH is also involved in regulating final insect size. Here we elucidate the developmental mechanism through which JH regulates body size in developing Drosophila larvae by genetically ablating the JH-producing organ, the corpora allata (CA). We found that larvae that lack CA pupariated at smaller sizes than control larvae due to a reduced larval growth rate. Neither the timing of the metamorphic molt nor the duration of larval growth was affected by the loss of JH. Further, we show that the effects of JH on growth rate are dependent on the forkhead box O transcription factor (FOXO), which is negatively regulated by the insulinsignaling pathway. Larvae that lacked the CA had elevated levels of FOXO activity, whereas a loss-of-function mutation of FOXO rescued the effects of CA ablation on final body size. Finally, the effect of JH on growth appears to be mediated, at least in part, via ecdysone synthesis in the prothoracic gland. These results indicate a role of JH in regulating growth rate via the ecdysone-and insulin-signaling pathways.T o correctly regulate their body size, animals control both the rate and duration of their growth. Canonically, growth rate and growth duration have been thought of as separate processes regulated by independent signaling pathways. In insects, the hormones ecdysone and juvenile hormone (JH) control the timing of the metamorphic transition and hence growth duration (1). The conserved insulin/insulin-like growth factor signaling (IIS) and target of rapamycin (TOR) pathways regulate growth rate (1). Recent evidence in Drosophila melanogaster indicates, however, that IIS and TOR signaling regulate ecdysone synthesis (2-5), whereas ecdysone antagonizes IIS (2, 6). This interaction between the mechanisms that regulate growth duration and those that control growth rate appears to coordinate the two processes, and may be a general feature of size regulation. To test this hypothesis, we explored whether JH also regulates growth rate in Drosophila.In the tobacco hornworm Manduca sexta, JH regulates growth duration by regulating the hormonal response to critical weight, a size checkpoint used to determine when to end growth and begin metamorphosis (7). A decline in circulating JH initiates the first step in the hormonal cascade that begins with attainment of critical weight, and ends, after a terminal growth period (TGP), in the rise in circulating ecdysone that stops body growth (8-10). Starvation maintains high rates of JH synthesis in the JH-producing tissue, the corpora allata (CA) (9), and delays the critical weight transition (8). Removal of the CA (CAX) causes larvae to reach critical weight earlier than normal and at a smaller size (8, 11). Application of JH suppresses the critical weight transition and delays metamorphosis, resulting in larger size (8).Intriguingly, recent studies show that, like CAX Manduca, CAX Drosophila larvae are smaller ...

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Sex-Specific Weight Loss Mediates Sexual Size Dimorphism in Drosophila melanogaster

Cited by 82 publications

References 41 publications

Effect of genomic deficiencies on sexual size dimorphism through modification of developmental time in Drosophila melanogaster

Effect of genomic deficiencies on sexual size dimorphism through modification of developmental time in Drosophila melanogaster

Temperature-size rule is mediated by thermal plasticity of critical size inDrosophila melanogaster

Juvenile hormone regulates body size and perturbs insulin signaling in Drosophila

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