Antagonistic Actions of Ecdysone and Insulins Determine Final Size in
            <i>Drosophila</i>

Colombani, Julien; Bianchini, Laurence; Layalle, Sophie; Pondeville, Emilie; Dauphin‐Villemant, Chantal; Antoniewski, Christophe; Carré, Clément; Noselli, Stéphane; Léopold, Pierre

doi:10.1126/science.1119432

Cited by 568 publications

(666 citation statements)

References 18 publications

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Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

“…Genetic alterations to enhance PI3K signaling in prothoracic glands of D. melanogaster cause the glands to grow to a size that is larger than normal (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). Paradoxically, the larvae with these larger glands produce adult flies that are smaller in size (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). The cause of the smaller adult size seems to be due to the larger glands secreting ecdysone earlier than they normally would (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005).…”

Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

“…Paradoxically, the larvae with these larger glands produce adult flies that are smaller in size (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). The cause of the smaller adult size seems to be due to the larger glands secreting ecdysone earlier than they normally would (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). Conversely, when PI3K signaling is genetically modified to be down-regulated in the prothoracic glands, the adult flies are larger in size (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005).…”

Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

“…The cause of the smaller adult size seems to be due to the larger glands secreting ecdysone earlier than they normally would (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). Conversely, when PI3K signaling is genetically modified to be down-regulated in the prothoracic glands, the adult flies are larger in size (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). This is likely due to the prothoracic glands secreting ecdysone later than they normally would, so the larvae are able to grow for a longer period of time.…”

Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

“…More recently other hormones, such as insulin, have received attention as regulators of metamorphosis (Caldwell et al, 2005;Colombani et al, 2005;Mirth et al, 2005). It is unclear how, specifically, insulin-like hormones interact with classical regulators of insect metamorpho sis such as ecdysone.…”

Section: Introductionmentioning

confidence: 99%

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Nutritional sensitivity of fifth instar prothoracic glands in the tobacco hornworm, Manduca sexta

Walsh

Smith

2011

Journal of Insect Physiology

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The tobacco hornworm, Manduca sexta, has been a useful model for studying insect endocrinology. In M. sexta the majority of growth occurs during the fifth (final) larval stage. This growth is concurrent with endocrine changes that lead to a metamorphic molt. Past research has focused on the interplay of three growth hormones: juvenile hormone (JH), prothoracicotropic hormone (PTTH) and ecdysone, in regulating metamorphosis. The prothoracic glands, source of ecdysteroid molting hormones in insects, play a crucial role in coordinating growth. Insulin/insulin-like growth factor (IGF) signaling has been shown to regulate growth and secretion of steroidogenic tissues in both vertebrates and invertebrates, but it had yet to be well-characterized in M. sexta.In this dissertation I examined the role of insulin-directed growth in prothoracic glands during both normal larval development and in response to nutrient deprivation. In particular, I predicted that in response to a reduction in nutrients, the prothoracic glands would stop growing and ecdysone secretion would be reduced. Changes were assessed in actin abundance and in two nutritionally sensitive transcripts, insulin receptor and 4EBP.Actin abundance in prothoracic glands increased in the first four days of this stage, demo nstrating significant growth. Actin decreased in glands from starved larvae, indicating a cessation of growth. Both insulin receptor and 4EBP transcript were present during normal larval development. As expected, both insulin receptor and 4EBP transcript increased in response to starvation. This research was the first demonstration of insulin signaling in prothoracic glands of fifth instar M. sexta larvae, and revealed nutritional sensitivity of the prothoracic glands. 5Finally, ecdysone assays were conducted to determine the impact of nutrition on glandular secretory capacity. Starved larvae were unable to secrete as much ecdysone as fed controls. Injections of insulin were unable to rescue the ability of the glands to secrete high levels of ecdysone. This demonstrated that although insulin signaling was correlated with normal growth of the glands, insulin is not sufficient to impact the ability of the glands to secrete ecdysone in the absence of nutrie nts. 6 This thesis is dedicated to my parents,Robert and Angela Walsh, whose love and support made this dissertation possible.

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Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

Section: Insulin Signaling and Growth In Insectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nutritional sensitivity of fifth instar prothoracic glands in the tobacco hornworm, Manduca sexta

Walsh

Smith

2011

Journal of Insect Physiology

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Drosophila ataxin‐2 gene encodes two differentially expressed isoforms and its function in larval fat body is crucial for development of peripheral tissues

et al. 2016

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Different isoforms of ataxin‐2 are predicted in Drosophila and may underlie different cellular processes. Here, we validated the isoforms B and C of Drosophila ataxin‐2 locus (dAtx2), which we found to be expressed in various tissues and at different levels during development. dAtx2‐B mRNA was detected at low amounts during all developmental stages, whereas dAtx2‐C mRNA levels increase by eightfold from L3 to pupal–adult stages. Higher amounts of dAtx2‐B protein were detected in embryos, while dAtx2‐C protein was also expressed in higher levels in pupal–adult stages, indicating post‐transcriptional control for isoform B and transcription induction for isoform C, respectively. Moreover, in the fat body of L3 larvae dAtx2‐C, but not dAtx2‐B, accumulates in cytoplasmic foci that colocalize with sec23, a marker of endoplasmic reticulum exit sites (ERES). Interestingly, animals subjected to selective knockdown of dAtx2 in the larval fat body do not complete metamorphosis and die at the third larval stage or early puparium. Additionally, larvae knocked down for dAtx2, grown at 29 °C, are significantly smaller than control animals due to reduction in DNA replication and cell growth, which are consistent with the decreased levels of phosphorylated‐AKT observed in the fat body. Based on the localization of ataxin‐2 (dAtx2‐C) in ERESs, and on the phenotypes observed by dAtx2 knockdown in the larval fat body, we speculate a possible role for this protein in processes that regulate ERES formation. These data provide new insights into the biological function of ataxin‐2 with potential relevance to neurodegenerative diseases.

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Role of EFAs/PUFAs in Brain Growth and Development and Pathophysiology of the Metabolic Syndrome

Das¹

2010

Metabolic Syndrome Pathophysiology

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Antagonistic Actions of Ecdysone and Insulins Determine Final Size in Drosophila

Cited by 568 publications

References 18 publications

Nutritional sensitivity of fifth instar prothoracic glands in the tobacco hornworm, Manduca sexta

Nutritional sensitivity of fifth instar prothoracic glands in the tobacco hornworm, Manduca sexta

Drosophila ataxin‐2 gene encodes two differentially expressed isoforms and its function in larval fat body is crucial for development of peripheral tissues

Role of EFAs/PUFAs in Brain Growth and Development and Pathophysiology of the Metabolic Syndrome

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