Ecdysone signaling cascade and regulation ofDrosophila metamorphosis

Baehrecke, Eric H.

doi:10.1002/(sici)1520-6327(1996)33:3/4<231::aid-arch5>3.0.co;2-v

Cited by 69 publications

(7 citation statements)

References 64 publications

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“…For example, Syncrip can be detected in many neuroblasts by 60 hr, whereas Broad appears slightly later at ~72 hr, and E93 is only detected much later at ~96 hr, by which time Broad is low. This staggered expression of ecdysone target genes is reminiscent of early and late ecdysone-inducible genes in other tissues (Baehrecke, 1996). In addition, for any particular temporal factor there are always some neuroblasts expressing it prior to others, but not in an obvious pattern.…”

Section: Discussionmentioning

confidence: 99%

Steroid hormone induction of temporal gene expression in Drosophila brain neuroblasts generates neuronal and glial diversity

Syed

Mark

Doe

2017

eLife

131

133

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An important question in neuroscience is how stem cells generate neuronal diversity. During Drosophila embryonic development, neural stem cells (neuroblasts) sequentially express transcription factors that generate neuronal diversity; regulation of the embryonic temporal transcription factor cascade is lineage-intrinsic. In contrast, larval neuroblasts generate longer ~50 division lineages, and currently only one mid-larval molecular transition is known: Chinmo/Imp/Lin-28+ neuroblasts transition to Syncrip+ neuroblasts. Here we show that the hormone ecdysone is required to down-regulate Chinmo/Imp and activate Syncrip, plus two late neuroblast factors, Broad and E93. We show that Seven-up triggers Chinmo/Imp to Syncrip/Broad/E93 transition by inducing expression of the Ecdysone receptor in mid-larval neuroblasts, rendering them competent to respond to the systemic hormone ecdysone. Importantly, late temporal gene expression is essential for proper neuronal and glial cell type specification. This is the first example of hormonal regulation of temporal factor expression in Drosophila embryonic or larval neural progenitors.DOI: http://dx.doi.org/10.7554/eLife.26287.001

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Section: Discussionmentioning

confidence: 99%

Steroid hormone induction of temporal gene expression in Drosophila brain neuroblasts generates neuronal and glial diversity

Syed

Mark

Doe

2017

eLife

131

133

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“…Ecdysteroid hormones, such as the major forms 20E and ponasterone A (PoA), bind to the ligand-binding domain of the EcR and activate the expression of primary early ecdysteroid responsive genes, such as E75 and E74 and early late genes such as HR3 and HR4 (114,115) (see also reviews by (116,117)). These transcriptional regulators drive the "late genes" responsible for metamorphosis, moulting, and/or ovarian development (114,(118)(119)(120). For ligand binding, the EcR forms a heterodimer with the retinoid-X-receptor (RXR), the ortholog of the insect ultraspiracle (121).…”

Section: Enzyme Synthesis and Inactivationmentioning

confidence: 99%

A Crab Is Not a Fish: Unique Aspects of the Crustacean Endocrine System and Considerations for Endocrine Toxicology

2021

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Crustaceans—and arthropods in general—exhibit many unique aspects to their physiology. These include the requirement to moult (ecdysis) in order to grow and reproduce, the ability to change color, and multiple strategies for sexual differentiation. Accordingly, the endocrine regulation of these processes involves hormones, receptors, and enzymes that differ from those utilized by vertebrates and other non-arthropod invertebrates. As a result, environmental chemicals known to disrupt endocrine processes in vertebrates are often not endocrine disruptors in crustaceans; while, chemicals that disrupt endocrine processes in crustaceans are often not endocrine disruptors in vertebrates. In this review, we present an overview of the evolution of the endocrine system of crustaceans, highlight endocrine endpoints known to be a target of disruption by chemicals, and identify other components of endocrine signaling that may prove to be targets of disruption. This review highlights that crustaceans need to be evaluated for endocrine disruption with consideration of their unique endocrine system and not with consideration of the endocrine system of vertebrates.

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“…However, mutant larvae are unable to grow; they retain a first instar larva size (<0.5mg) and fail to pupariate even after ten days of larval life (Figure. 1B). The ecdysone pathway, a steroid hormone controlling larval moulting (Baehrecke, 1996;Yamanaka, Rewitz and O'Connor, 2013), appears unaffected with the Ecdysone-induced protein 75B (E75B), the Prothoracicotropic hormone (PTTH), Phantom (Phm) and Disembodied (Dib) being expressed within wild-type ranges ( Figures S2A-E). Furthermore, the insulin receptor (dInr) and the Drosophila insulin-like peptide 2 (Dilp2) are upregulated to counteract the lack of growth ( Figures S2F and S2G).…”

Section: Mir-1010 In Contrast To Its Host Gene Skip Is Indispensablmentioning

confidence: 99%

The mirtron miR-1010 functions in concert with its host gene SKIP to maintain synaptic homeostasis

Amourda

2018

Preprint

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Main textMicroRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally regulate gene expression in nearly all cellular pathways 1,2 . Recently, studies have revealed the existence of a non-canonical miRNA maturation pathway 3-5 , whose miRNAs, named mirtrons, arise by splicing of an intron from a host gene 6 . A plethora of introns have been inferred as potential mirtrons 7-9 , yet few have been experimentally validated and their functions, particularly in relation to their host genes, remain poorly understood 10,11 .Here, we show that the mirtron miR-1010 downregulates the nicotinic acetylcholine receptor β2 (nAcRβ2) and subsequently maintains synaptic homeostasis within an optimal range. We found that larvae lacking miR-1010 are unable to properly grow and pupariate. Increase of cortical nAcRβ2 mediated by neural activity elevates the level of intracellular calcium (Ca 2+ ). This high Ca 2+ level activates the calcium/calmodulindependent kinase II (CaMKII) and, further downstream, the transcription factor Adf-1.We reveal that Adf-1 triggers the expression of SKIP, the host gene of miR-1010. SKIP tempers synaptic potential by regulating Shal, a potassium voltage-gated channel protein. MiR-1010 reduces the mRNA level of nAcRβ2 to prevent synaptic potentials from overshooting their optimal range. Our results demonstrate how a mirtron, in concert with its host gene, contributes to maintaining homeostasis.Since their discovery more than two decades ago 12,13 , miRNAs have been established as key cellular micromanagers. Canonical miRNAs are genetically encoded short (18-22 nucleotides) hairpin structures that are processed, after transcription, by the Drosha/Pasha

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Ecdysone signaling cascade and regulation ofDrosophila metamorphosis

Cited by 69 publications

References 64 publications

Steroid hormone induction of temporal gene expression in Drosophila brain neuroblasts generates neuronal and glial diversity

Steroid hormone induction of temporal gene expression in Drosophila brain neuroblasts generates neuronal and glial diversity

A Crab Is Not a Fish: Unique Aspects of the Crustacean Endocrine System and Considerations for Endocrine Toxicology

The mirtron miR-1010 functions in concert with its host gene SKIP to maintain synaptic homeostasis

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