Hormonal and nutritional regulation of insect fat body development and function

Liu, Ying; Liu, Hanhan; Liu, Shumin; Wang, Sheng; Jiang, Rong‐Jing; Li, Sheng

doi:10.1002/arch.20290

Cited by 129 publications

(95 citation statements)

References 50 publications

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“…Bioenergetic studies clearly indicated UCP function in mitochondria isolated from both G. cocquereliana leg muscle and fat body tissue, the latter being an insect analogue tissue to vertebrate adipose tissue and liver functioning as a major organ for nutrient storage and energy metabolism (Liu et al 2009). The activity of the G. cocquereliana uncoupling protein (GcUCP) is stimulated by free fatty acids and inhibited by purine nucleotides (GTP).…”

Section: Discussionmentioning

confidence: 99%

Identification and characterization of uncoupling protein 4 in fat body and muscle mitochondria from the cockroach Gromphadorhina cocquereliana

Słocińska

Antos-Krzemińska

Rosiński

et al. 2011

J Bioenerg Biomembr

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We have identified and characterized an uncoupling protein in mitochondria isolated from leg muscle and from fat body, an insect analogue tissue of mammalian liver and adipose tissue, of the cockroach Gromphadorhina coquereliana (GcUCP). This is the first functional characterization of UCP activity in isolated insect mitochondria. Bioenergetic studies clearly indicate UCP function in both insect tissues. In resting (non-phosphorylating) mitochondria, cockroach GcUCP activity was stimulated by the addition of micromolar concentrations of palmitic acid and inhibited by the purine nucleotide GTP. Moreover, in phosphorylating mitochondria, GcUCP activity was able to divert energy from oxidative phosphorylation. Functional studies indicate a higher activity of GcUCP-mediated uncoupling in cockroach muscle mitochondria compared to fat body mitochondria. GcUCP activation by palmitic acid resulted in a decrease in superoxide anion production, suggesting that protection against mitochondrial oxidative stress may be a physiological role of UCPs in insects. GcUCP protein was immunodetected using antibodies raised against human UCP4 as a single band of around 36 kDa. GcUCP protein expression in cockroach muscle mitochondria was significantly higher compared to mitochondria isolated from fat body. LC-MS/MS analyses revealed 100% sequence identities for peptides obtained from GcUCP to UCP4 isoforms from D. melanogaster (the highest homology), human, rat or other insect mitochondria. Therefore, it can be proposed that cockroach GcUCP corresponds to the UCP4 isoforms of other animals.

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Section: Discussionmentioning

confidence: 99%

Identification and characterization of uncoupling protein 4 in fat body and muscle mitochondria from the cockroach Gromphadorhina cocquereliana

Słocińska

Antos-Krzemińska

Rosiński

et al. 2011

J Bioenerg Biomembr

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“…27,28,[34][35][36]60 Moreover, the 20E-induced autophagy and endocytosis crosstalk with each other and share some regulatory components, including PIK3C3/ VPS34. 61 The fat body functions as a major organ for nutrient storage and energy metabolism in insects; 22,32,33 therefore, the function of autophagy in exploiting remaining nutrients should be particularly important in this insect adipose tissue.…”

Section: E Upregulatesmentioning

confidence: 99%

“…It is considered to be the central organ that integrates and coordinates different hormonal and nutritional signals for regulating insect development and metamorphosis. 20,32,33 In the fat body of two lepidopteran species and Drosophila, 20E-induced developmental autophagy progressively occurs during the larvalprepupal transition, 21,27,28,[34][35][36][37] and in the Drosophila fat body, EcR is required for 20E to induce autophagy. 21 We have previously determined that in the Bombyx fat body, 20E upregulates apoptosis genes to induce some apoptotic events.…”

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confidence: 99%

20-hydroxyecdysone upregulatesAtggenes to induce autophagy in the Bombyx fat body

Tian¹,

et al. 2013

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Autophagy is finely regulated at multiple levels and plays crucial roles in development and disease. in the fat body of the silkworm, Bombyx mori, autophagy occurs and Atg gene expression peaks during the nonfeeding molting and pupation stages when the steroid hormone (20-hydroxyecdysone; 20E) is high. injection of 20E into the feeding larvae upregulated Atg genes and reduced torC1 activity resulting in autophagy induction in the fat body. Conversely, rnAi knockdown of the 20E receptor partner (USP) or targeted overexpression of a dominant negative mutant of the 20E receptor (EcR DN ) in the larval fat body reduced autophagy and downregulated the Atg genes, confirming the importance of 20E-induction of Atg gene expression during pupation. Moreover, in vitro treatments of the larval fat body with 20E upregulated the Atg genes. Five Atg genes were potentially 20E primary-responsive, and a 20E response element was identified in the Atg1 (ortholog of human ULK1) promoter region. Furthermore, rnAi knockdown of 4 key genes (namely Br-C, E74, HR3 and βftz-F1) in the 20E-triggered transcriptional cascade reduced autophagy and downregulated Atg genes to different levels. taken together, we conclude that in addition to blocking torC1 activity for autophagosome initiation, 20E upregulates Atg genes to induce autophagy in the Bombyx fat body.

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“…1E). During the larval-pupal metamorphosis of Drosophila, the fat body undergoes a remodeling process but remains in the posterior part of the pupa (Nelliot et al, 2006;Liu et al, 2009). The posterior portion of the JH-deficient pupae often appeared to be empty, suggesting that JH has an important role in the control of fat body development during the larval-pupal transition.…”

Section: Research Articlementioning

confidence: 99%

Juvenile hormone counteracts the bHLH-PAS transcription factors MET and GCE to prevent caspase-dependent programmed cell death inDrosophila

et al. 2009

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Juvenile hormone (JH) regulates many developmental and physiological events in insects, but its molecular mechanism remains conjectural. Here we report that genetic ablation of the corpus allatum cells of the Drosophila ring gland (the JH source) resulted in JH deficiency, pupal lethality and precocious and enhanced programmed cell death (PCD) of the larval fat body. In the fat body of the JH-deficient animals, Dronc and Drice, two caspase genes that are crucial for PCD induced by the molting hormone 20-hydroxyecdysone (20E), were significantly upregulated. These results demonstrated that JH antagonizes 20E-induced PCD by restricting the mRNA levels of Dronc and Drice. The antagonizing effect of JH on 20E-induced PCD in the fat body was further confirmed in the JH-deficient animals by 20E treatment and RNA interference of the 20E receptor EcR. Moreover, MET and GCE, the bHLH-PAS transcription factors involved in JH action, were shown to induce PCD by upregulating Dronc and Drice. In the Met-and gce-deficient animals, Dronc and Drice were downregulated, whereas in the Met-overexpression fat body, Dronc and Drice were significantly upregulated leading to precocious and enhanced PCD, and this upregulation could be suppressed by application of the JH agonist methoprene. For the first time, we demonstrate that JH counteracts MET and GCE to prevent caspase-dependent PCD in controlling fat body remodeling and larval-pupal metamorphosis in Drosophila.

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Hormonal and nutritional regulation of insect fat body development and function

Cited by 129 publications

References 50 publications

Identification and characterization of uncoupling protein 4 in fat body and muscle mitochondria from the cockroach Gromphadorhina cocquereliana

Identification and characterization of uncoupling protein 4 in fat body and muscle mitochondria from the cockroach Gromphadorhina cocquereliana

20-hydroxyecdysone upregulatesAtggenes to induce autophagy in the Bombyx fat body

Juvenile hormone counteracts the bHLH-PAS transcription factors MET and GCE to prevent caspase-dependent programmed cell death inDrosophila

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