scholarly journals Antagonistic actions of juvenile hormone and 20-hydroxyecdysone within the ring gland determine developmental transitions in Drosophila

2017 ◽  
Vol 115 (1) ◽  
pp. 139-144 ◽  
Author(s):  
Suning Liu ◽  
Kang Li ◽  
Yue Gao ◽  
Xi Liu ◽  
Weiting Chen ◽  
...  
Keyword(s):  
Juvenile Hormone ◽  
Cross Talk ◽  
Steroid Hormone ◽  
Corpus Allatum ◽  
Prothoracic Gland ◽  
Transcription Factor Gene ◽  
Developmental Transitions ◽  
Larval Stages ◽  
Ring Gland ◽  
Insect Metamorphosis

In both vertebrates and insects, developmental transition from the juvenile stage to adulthood is regulated by steroid hormones. In insects, the steroid hormone, 20-hydroxyecdysone (20E), elicits metamorphosis, thus promoting this transition, while the sesquiterpenoid juvenile hormone (JH) antagonizes 20E signaling to prevent precocious metamorphosis during the larval stages. However, not much is known about the mechanisms involved in cross-talk between these two hormones. In this study, we discovered that in the ring gland (RG) of Drosophila larvae, JH and 20E control each other’s biosynthesis. JH induces expression of a Krüppel-like transcription factor gene Kr-h1 in the prothoracic gland (PG), a portion of the RG that produces the 20E precursor ecdysone. By reducing both steroidogenesis autoregulation and PG size, high levels of Kr-h1 in the PG inhibit ecdysteriod biosynthesis, thus maintaining juvenile status. JH biosynthesis is prevented by 20E in the corpus allatum, the other portion of the RG that produces JH, to ensure the occurrence of metamorphosis. Hence, antagonistic actions of JH and 20E within the RG determine developmental transitions in Drosophila. Our study proposes a mechanism of cross-talk between the two major hormones in the regulation of insect metamorphosis.

scholarly journals Torso-like is a component of the hemolymph and regulates the insulin signalling pathway in Drosophila

2018 ◽  
Author(s):  
Michelle A. Henstridge ◽  
Lucinda Aulsebrook ◽  
Takashi Koyama ◽  
Travis K. Johnson ◽  
James C. Whisstock ◽  
...  
Keyword(s):  
Body Size ◽  
Insulin Signalling ◽  
Steroid Hormone ◽  
The Body ◽  
Signalling Pathway ◽  
Prothoracic Gland ◽  
Signalling Pathways ◽  
Mature Adult ◽  
Developmental Transitions ◽  
Insulin Signalling Pathway

ABSTRACTIn Drosophila key developmental transitions are governed by the steroid hormone ecdysone. A number of neuropeptide-activated signalling pathways control ecdysone production in response to environmental signals, including the insulin signalling pathway, which regulates ecdysone production in response to nutrition. Here, we find that the Membrane Attack Complex/Perforin-like protein Torso-like, best characterised for its role in activating the Torso receptor tyrosine kinase in early embryo patterning, also regulates the insulin signalling pathway in Drosophila. We previously reported that the small body size and developmental delay phenotypes of torso-like null mutants resemble those observed when insulin signalling is reduced. Here we report that, in addition to growth defects, torso-like mutants also display metabolic and nutritional plasticity phenotypes characteristic of mutants with impaired insulin signalling. We further find that in the absence of torso-like the expression of insulin-like peptides is increased, as is their accumulation in the insulin-producing cells. Finally, we show that Torso-like is a component of the hemolymph and that it is required in the prothoracic gland to control developmental timing and body size. Taken together, our data suggest that the secretion of Torso-like from the prothoracic gland influences the activity of insulin signalling throughout the body in Drosophila.ARTICLE SUMMARYIn many animals distinct developmental transitions are crucial for the coordinated progression from the juvenile stage to adulthood. In Drosophila, the transition from an immature larva into a reproductively mature adult is controlled by the steroid hormone ecdysone. Several neuropeptide-activated signalling pathways, including the insulin signalling pathway, regulate ecdysone production in response to environmental cues. Here we find that the perforin-like protein Torso-like regulates the insulin signalling pathway. We show that Torso-like is secreted into circulation where it acts to influence insulin-like peptide activity, revealing a novel mechanism for the regulation of insulin signalling in Drosophila.

scholarly journals Autocrine regulation of ecdysone synthesis by β3-octopamine receptor in the prothoracic gland is essential for Drosophila metamorphosis

2015 ◽  
Vol 112 (5) ◽  
pp. 1452-1457 ◽  
Author(s):  
Yuya Ohhara ◽  
Yuko Shimada-Niwa ◽  
Ryusuke Niwa ◽  
Yasunari Kayashima ◽  
Yoshiki Hayashi ◽  
...  
Keyword(s):  
Body Size ◽  
Signaling Pathways ◽  
G Protein ◽  
Steroid Hormone ◽  
Prothoracic Gland ◽  
Autocrine Signaling ◽  
Developmental Transitions ◽  
Autocrine Regulation ◽  
Octopamine Receptor ◽  
G Protein Coupled

In Drosophila, pulsed production of the steroid hormone ecdysone plays a pivotal role in developmental transitions such as metamorphosis. Ecdysone production is regulated in the prothoracic gland (PG) by prothoracicotropic hormone (PTTH) and insulin-like peptides (Ilps). Here, we show that monoaminergic autocrine regulation of ecdysone biosynthesis in the PG is essential for metamorphosis. PG-specific knockdown of a monoamine G protein-coupled receptor, β3-octopamine receptor (Octβ3R), resulted in arrested metamorphosis due to lack of ecdysone. Knockdown of tyramine biosynthesis genes expressed in the PG caused similar defects in ecdysone production and metamorphosis. Moreover, PTTH and Ilps signaling were impaired by Octβ3R knockdown in the PG, and activation of these signaling pathways rescued the defect in metamorphosis. Thus, monoaminergic autocrine signaling in the PG regulates ecdysone biogenesis in a coordinated fashion on activation by PTTH and Ilps. We propose that monoaminergic autocrine signaling acts downstream of a body size checkpoint that allows metamorphosis to occur when nutrients are sufficiently abundant.

Delayed Effects of Juvenile Hormone on Insect Metamorphosis are mediated by the Corpus Allatum

Nature ◽  
1972 ◽  
Vol 237 (5356) ◽  
pp. 458-458 ◽  
Author(s):  
LYNN M. RIDDIFORD ◽  
JAMES W. TRUMAN
Keyword(s):  
Juvenile Hormone ◽  
Corpus Allatum ◽  
Delayed Effects ◽  
Insect Metamorphosis

The dare gene: steroid hormone production, olfactory behavior, and neural degeneration in Drosophila

Development ◽  
1999 ◽  
Vol 126 (20) ◽  
pp. 4591-4602 ◽  
Author(s):  
M.R. Freeman ◽  
A. Dobritsa ◽  
P. Gaines ◽  
W.A. Segraves ◽  
J.R. Carlson
Keyword(s):  
Nervous System ◽  
Steroid Hormones ◽  
Steroid Hormone ◽  
Larval Instar ◽  
Hormone Production ◽  
Ring Gland ◽  
Olfactory Stimuli ◽  
Steroid Hormone Signaling ◽  
Adrenodoxin Reductase ◽  
Strength Result

Steroid hormones mediate a wide variety of developmental and physiological events in insects, yet little is known about the genetics of insect steroid hormone biosynthesis. Here we describe the Drosophila dare gene, which encodes adrenodoxin reductase (AR). In mammals, AR plays a key role in the synthesis of all steroid hormones. Null mutants of dare undergo developmental arrest during the second larval instar or at the second larval molt, and dare mutants of intermediate severity are delayed in pupariation. These defects are rescued to a high degree by feeding mutant larvae the insect steroid hormone 20-hydroxyecdysone. These data, together with the abundant expression of dare in the two principal steroid biosynthetic tissues, the ring gland and the ovary, argue strongly for a role of dare in steroid hormone production. dare is the first Drosophila gene shown to encode a defined component of the steroid hormone biosynthetic cascade and therefore provides a new tool for the analysis of steroid hormone function. We have explored its role in the adult nervous system and found two striking phenotypes not previously described in mutants affected in steroid hormone signaling. First, we show that mild reductions of dare expression cause abnormal behavioral responses to olfactory stimuli, indicating a requirement for dare in sensory behavior. Then we show that dare mutations of intermediate strength result in rapid, widespread degeneration of the adult nervous system.

scholarly journals Involvement of steroid hormone and growth factor cross-talk in endocrine response in breast cancer.

1999 ◽  
pp. 373-387 ◽  
Author(s):  
R I Nicholson ◽  
R A McClelland ◽  
J F Robertson ◽  
J M Gee
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cross Talk ◽  
Therapeutic Response ◽  
Steroid Hormone ◽  
Common Element ◽  
Growth Factor Signaling ◽  
Endocrine Response ◽  
Resistant Phenotype ◽  
Lines Of Evidence

Multiple lines of evidence implicate steroid hormone and growth factor cross-talk as a modulator of endocrine response in breast cancer and that aberrations in growth factor signaling pathways are a common element in the endocrine resistant phenotype. Delineation of these relationships is thus an important diagnostic goal in cancer research, while the targeting of aberrant growth factor signaling holds the promise of improving therapeutic response rates.

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