Abstract
Literature on the question whether the juvenile stage of vertebrates is hormonally regulated is scarce. It seems to be intuitively assumed that this stage of development is automated, and does not require any specific hormone(s). Such reasoning mimics the state of affairs in insects until it was shown that surgical removal of a tiny pair of glands in the head, the corpora allata, ended larval life and initiated metamorphosis. Decades later, the responsible hormone was found and named “juvenile hormone” (JH) because when present, it makes a larva molt into another larval stage. JH is a simple ester of farnesol, a sesquiterpenoid present in all eukaryotes. Whereas vertebrates do not have an anatomical counterpart of the corpora allata, their tissues do contain farnesol-like sesquiterpenoids (FLS). Some display typical JH activity when tested in appropriate insect bioassays. Some FLS are intermediates in the biosynthetic pathway of cholesterol, a compound that insects and nematodes (=Ecdysozoa) cannot synthesize by themselves. They ingest it as a vitamin. Until a recent (2014) reexamination of the basic principle underlying insect metamorphosis, it had been completely overlooked that the Ca2+-pump (SERCA) blocker thapsigargin is a sesquiterpenoid that mimics the absence of JH in inducing apoptosis. In our opinion, being in the juvenile state is primarily controlled by endogenous FLS that participate in controlling the activity of Ca2+-ATPases in the sarco(endo)plasmic reticulum (SERCAs), not only in insects but in all eukaryotes. Understanding the control mechanisms of being in the juvenile state may boost research not only in developmental biology in general, but also in diseases that develop after the juvenile stage, e.g., Alzheimer’s disease. It may also help to better understand some of the causes of obesity, a syndrome that holometabolous last larval insects severely suffer from, and for which they found a very drastic but efficient solution, namely metamorphosis.
Highlights
All animals, plants and fungi pass through a juvenile stage before becoming reproductively active and becoming aged
Because insects and nematodes either lost or never had the gene coding for the enzyme squalene synthase that converts squalene into cholesterol, they cannot make cholesterol by themselves. They solved this problem by ingesting cholesterol as a vitamin and by using a farnesol ester, namely juvenile hormone (JH) as a circulating hormone to control at least one of the components of the Ca2+-homeostasis system, namely the SERCA-pump system
This is due to the fact that unlike in insects where – in larvae – farnesol and JH are only synthesized in the corpora allata, farnesol-like sesquiterpenoids (FLS) are present in all cells of the vertebrate body (Table 1, see later)
Summary
Plants and fungi pass through a juvenile stage before becoming reproductively active and becoming aged. It is more likely that their key components have been well conserved in evolution, rather than that deuterostomes (to which vertebrates belong) “all of a sudden” invented a completely new strategy for generating and temporarily maintaining a juvenile state It is well-known that insects, which are protostomes, use JH as their juvenilizing agent. Because insects and nematodes either lost or never had the gene coding for the enzyme squalene synthase that converts squalene (that is formed from FPP) into cholesterol, they cannot make cholesterol by themselves They solved this problem by ingesting cholesterol as a vitamin and by using a farnesol ester, namely JH as a circulating hormone to control at least one of the components of the Ca2+-homeostasis system, namely the SERCA-pump system
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