The essence of insect metamorphosis and aging: Electrical rewiring of cells driven by the principles of juvenile hormone-dependent Ca2+-homeostasis

Loof, Arnold De; Haes, Wouter De; Janssen, Tom; Schoofs, Liliane

doi:10.1016/j.ygcen.2014.01.009

Cited by 26 publications

(67 citation statements)

References 106 publications

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“…According to De Loof et al (2014), a low cytoplasmic Ca 2C concentration is causal to maintaining the larval status of holometabolous insects. At least some of the proteins that constitute the Ca 2C homeostasis system have a binding site for sesquiterpenoids, JH being one of them.…”

Section: Met1 Promotes Krh1 Transcription To Maintain the Larval Statusmentioning

confidence: 99%

“…Indeed, at least some isoforms of Ca 2C -ATPase have a binding site for farnesol-like sesquiterpenoids, the family of compounds to which JH belongs. These authors think that a low cytoplasmic Ca 2C concentration is causal to the status quo effect of JH (De Loof et al 2014). Met forms homodimers with Met or germ cell expressed (Gce) without hormone regulation in Drosophila (Godlewski et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Methoprene-tolerant 1 regulates gene transcription to maintain insect larval status

Zhao¹,

Liu²,

Li³

et al. 2014

Journal of Molecular Endocrinology

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Insect molting and metamorphosis are regulated by two hormones: 20-hydroxyecdysone (20E) and juvenile hormone (JH). The hormone 20E regulates gene transcription via the nuclear receptor EcR to promote metamorphosis, whereas JH regulates gene transcription via its intracellular receptor methoprene-tolerant (Met) to prevent larval-pupal transition. However, the function and mechanism of Met in various insect developments are not well understood. We propose that Met1 plays a key role in maintaining larval status not only by promoting JH-responsive gene transcription but also by repressing 20E-responsive gene transcription in the Lepidopteran insect Helicoverpa armigera. Met1 protein is increased during feeding stage and decreased during molting and metamorphic stages. Met1 is upregulated by JH III and a low concentration of 20E independently, but is downregulated by a high concentration of 20E. Knockdown of Met1 in larvae causes precocious pupation, decrease in JH pathway gene expression, and increase in 20E pathway gene expression. Met1 interacts with heat shock protein 90 and binds to JH response element to regulate Krü ppel homolog 1 transcription in JH III induction. Met1 interacts with ultraspiracle protein 1 (USP1) to repress 20E transcription complex EcRB1/USP1 formation and binding to ecdysone response element. These data indicate that JH via Met1 regulates JH pathway gene expression and represses 20E pathway gene expression to maintain the larval status.

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Section: Met1 Promotes Krh1 Transcription To Maintain the Larval Statusmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Methoprene-tolerant 1 regulates gene transcription to maintain insect larval status

Zhao¹,

Liu²,

Li³

et al. 2014

Journal of Molecular Endocrinology

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“…It has been demonstrated that the Bombyx ovary might have the capacity to synthesize and accumulate vertebrate steroid hormones. It has been recently suggested that steroid hormones in both vertebrates and invertebrates may play a role in calcium homeostasis because calcium has a role in all cell types; the effect of E 2 could be cell-specific and not necessarily linked to the classical concept of reproduction in female system (De Loof et al, 2014;De Loof, 2015). The presence of sex steroids in invertebrates has been studied for many years and other findings can demonstrate the role of estrogen in the alteration of female-specific protein in the hemolymph and ovary in B. mori (Das and Ray, 2014a).…”

Section: Biological Role Of Vertebrate Hormones In Silkwormsmentioning

confidence: 99%

Vertebrate hormones in insects: the role of estrogen in silkworm – a review

Das¹

2016

Turk J Zool

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“…It served as the template for a figure in ' 'Orrenius et al (2003), Nature Reviews of Cell Biology 4, 552-556. It has already been used in a previous paper by De Loof et al (2014a). With copyright permission for both the figure and the legend from the publisher and from Orrenius.…”

Section: The Golgi System Is Also An Undervalued Player In Ca 2+ -Hommentioning

confidence: 99%

“…This pump is thought to be more related to the putative ancestral Ca 2+ pump than the SERCA. It is not sensitive to the sesquiterpenoid toxin thapsigargin indicating that, unlike (some isoforms of) SERCA it is not sesquiterpenoid (farnesol)-dependent for being active (De Loof et al, 2014a). Furthermore, subcompartments of the ER-Golgi complex that endogenously express SPCA1 are insensitive to agonists that produce inositol triphosphate (Vanoevelen et al, 2004).…”

Section: The Golgi System Is Also An Undervalued Player In Ca 2+ -Hommentioning

confidence: 99%

The essence of female–male physiological dimorphism: Differential Ca2+-homeostasis enabled by the interplay between farnesol-like endogenous sesquiterpenoids and sex-steroids? The Calcigender paradigm

Loof

2015

General and Comparative Endocrinology

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Ca(2+) is the most omnipresent pollutant on earth, in higher concentrations a real threat to all living cells. When [Ca(2+)]i rises above 100 nM (=resting level), excess Ca(2+) needs to be confined in the SER and mitochondria, or extruded by the different Ca(2+)-ATPases. The evolutionary origin of eggs and sperm cells has a crucial, yet often overlooked link with Ca(2+)-homeostasis. Because there is no goal whatsoever in evolution, gametes did neither originate "with the purpose" of generating a progeny nor of increasing fitness by introducing meiosis. The explanation may simply be that females "invented the trick" to extrude eggs from their body as an escape strategy for getting rid of toxic excess Ca(2+) resulting from a sex-hormone driven increased influx into particular cells and tissues. The production of Ca(2+)-rich milk, seminal fluid in males and all secreted proteins by eukaryotic cells may be similarly explained. This view necessitates an upgrade of the role of the RER-Golgi system in extruding Ca(2+). In the context of insect metamorphosis, it has recently been (re)discovered that (some isoforms of) Ca(2+)-ATPases act as membrane receptors for some types of lipophilic ligands, in particular for endogenous farnesol-like sesquiterpenoids (FLS) and, perhaps, for some steroid hormones as well. A novel paradigm, tentatively named "Calcigender" emerges. Its essence is: gender-specific physiotypes ensue from differential Ca(2+)-homeostasis enabled by genetic differences, farnesol/FLS and sex hormones. Apparently the body of reproducing females gets temporarily more poisoned by Ca(2+) than the male one, a selective benefit rather than a disadvantage.

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The essence of insect metamorphosis and aging: Electrical rewiring of cells driven by the principles of juvenile hormone-dependent Ca2+-homeostasis

Cited by 26 publications

References 106 publications

Methoprene-tolerant 1 regulates gene transcription to maintain insect larval status

Methoprene-tolerant 1 regulates gene transcription to maintain insect larval status

Vertebrate hormones in insects: the role of estrogen in silkworm – a review

The essence of female–male physiological dimorphism: Differential Ca2+-homeostasis enabled by the interplay between farnesol-like endogenous sesquiterpenoids and sex-steroids? The Calcigender paradigm

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