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"Insects Metamorphosis"
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The search for baby butterflies
\"Elinor, Ari and Olive are spending the day at the park with Ari's dad and his baby sister, Miri, who is just the cutest. The friends are split on what to do in the park: Ari suggests butterfly-watching, but Olive wants to hunt for caterpillars. Elinor wonders why they've never seen a baby butterfly before, and an insect investigation begins! The trio search high and low, but there's no sign of baby butterflies anywhere. A caterpillar catches Olive's eye, and the friends watch in awe as it disappears into a cocoon. But the real surprise comes when another cocoon starts to crack open, and a butterfly emerges! The mystery of the missing butterfly babies is solved! Eager entomologists will love this latest adventure as Elinor, Olive and Ari unravel another mystery of science and nature. By following their curiosity, making observations and creating connections, the three friends work together to learn something new about how the world works -- and have fun while they're at it! The back matter includes more fun facts about metamorphosis, a key vocabulary word and a simple activity for young scientists to explore further.\"-- Provided by publisher.
Book
Transcription factor E93 specifies adult metamorphosis in hemimetabolous and holometabolous insects
All immature animals undergo remarkable morphological and physiological changes to become mature adults. In winged insects, metamorphic changes either are limited to a few tissues (hemimetaboly) or involve a complete reorganization of most tissues and organs (holometaboly). Despite the differences, the genetic switch between immature and adult forms in both types of insects relies on the disappearance of the antimetamorphic juvenile hormone (JH) and the transcription factors Krüppel-homolog 1 (Kr-h1) and Broad-Complex (BR-C) during the last juvenile instar. Here, we show that the transcription factor E93 is the key determinant that promotes adult metamorphosis in both hemimetabolous and holometabolous insects, thus acting as the universal adult specifier. In the hemimetabolous insect Blattella germanica , BgE93 is highly expressed in metamorphic tissues, and RNA interference (RNAi)-mediated knockdown of BgE93 in the nymphal stage prevented the nymphal–adult transition, inducing endless reiteration of nymphal development, even in the absence of JH. We also find that BgE93 down-regulated BgKr-h1 and BgBR-C expression during the last nymphal instar of B. germanica , a key step necessary for proper adult differentiation. This essential role of E93 is conserved in holometabolous insects as TcE93 RNAi in Tribolium castaneum prevented pupal–adult transition and produced a supernumerary second pupa. In this beetle, TcE93 also represses expression of TcKr-h1 and TcBR-C during the pupal stage. Similar results were obtained in the more derived holometabolous insect Drosophila melanogaster , suggesting that winged insects use the same regulatory mechanism to promote adult metamorphosis. This study provides an important insight into the understanding of the molecular basis of adult metamorphosis.
Journal Article
The girl who drew butterflies : how Maria Merian's art changed science
\"Newbery-Honor winning author Joyce Sidman explores the extraordinary life and scientific discoveries of Maria Merian, who discovered the truth about metamorphosis and documented the science behind the mystery in this visual biography that features many original paintings by Maria herself.\"-- Provided by publisher.
Book
Juvenile Hormones and Juvenoids
Juvenile hormones (JHs) affect most stages of the insect life-cycle as well as their physiological functions. Juvenoids, manmade chemicals that mimic the actions of JHs, can be used to disrupt the endocrine system of insects, making them particularly suited as larvicides for the control of pest and disease vectoring insects. This book presents various modeling approaches and computational methods that can be used to study the mechanism of action of JHs in insects and to estimate the adverse effects and the environmental fate of juvenoids.
eBook
Regulation of metamorphosis in neopteran insects is conserved in the paleopteran Cloeon dipterum (Ephemeroptera)
In the Paleozoic era, more than 400 Ma, a number of insect groups continued molting after forming functional wings. Today, however, flying insects stop molting after metamorphosis when they become fully winged. The only exception is the mayflies (Paleoptera, Ephemeroptera), which molt in the subimago, a flying stage between the nymph and the adult. However, the identity and homology of the subimago still is underexplored. Debate remains regarding whether this stage represents a modified nymph, an adult, or a pupa like that of butterflies. Another relevant question is why mayflies have the subimago stage despite the risk of molting fragile membranous wings. These questions have intrigued numerous authors, but nonetheless, clear answers have not yet been found. By combining morphological studies, hormonal treatments, and molecular analysis in the mayfly Cloeon dipterum, we found answers to these old questions. We observed that treatment with a juvenile hormone analog in the last nymphal instar stimulated the expression of the Kr-h1 gene and reduced that of E93, which suppress and trigger metamorphosis, respectively. The regulation of metamorphosis thus follows the MEKRE93 pathway, as in neopteran insects. Moreover, the treatment prevented the formation of the subimago. These findings suggest that the subimago must be considered an instar of the adult mayfly. We also observed that the forelegs dramatically grow between the last nymphal instar, the subimago, and the adult. This necessary growth spread over the last two stages could explain, at least in part, the adaptive sense of the subimago.
Journal Article
MiR-2 family regulates insect metamorphosis by controlling the juvenile hormone signaling pathway
In 2009 we reported that depletion of Dicer-1, the enzyme that catalyzes the final step of miRNA biosynthesis, prevents metamorphosis in Blattella germanica . However, the precise regulatory roles of miRNAs in the process have remained elusive. In the present work, we have observed that Dicer-1 depletion results in an increase of mRNA levels of Krúñíóüüüppel homolog 1 (Kr-h1), a juvenile hormone-dependent transcription factor that represses metamorphosis, and that depletion of Kr-h1 expression in Dicer-1 knockdown individuals rescues metamorphosis. We have also found that the 3′UTR of Kr-h1 mRNA contains a functional binding site for miR-2 family miRNAs (for miR-2, miR-13a, and miR-13b). These data suggest that metamorphosis impairment caused by Dicer-1 and miRNA depletion is due to a deregulation of Kr-h1 expression and that this deregulation is derived from a deficiency of miR-2 miRNAs. We corroborated this by treating the last nymphal instar of B. germanica with an miR-2 inhibitor, which impaired metamorphosis, and by treating Dicer-1-depleted individuals with an miR-2 mimic to allow nymphal-to-adult metamorphosis to proceed. Taken together, the data indicate that miR-2 miRNAs scavenge Kr-h1 transcripts when the transition from nymph to adult should be taking place, thus crucially contributing to the correct culmination of metamorphosis.
Significance MicroRNAs are short, single-stranded RNAs that bind to target mRNAs and block their translation. Five years ago we observed in the cockroach Blattella germanica that general depletion of microRNAs prevents metamorphosis. This observation led to two key questions: Which microRNAs are involved in this action, and which target do they act on? The results reported herein show that the microRNAs involved are those of an miR-2 family (miR-2, miR-13a, and miR-13b), and the target is the transcription factor Krúñíóüppel homolog 1, a master repressor of insect metamorphosis. The data presented indicate that miR-2 microRNAs rapidly clear Krúñíóüüppel homolog 1 transcripts in the last nymphal instar, a process that is crucial for proper metamorphosis. This reveals the elegant mechanism of an miRNA family leading metamorphosis to its correct conclusion.
Journal Article
Krüppel-homolog 1 exerts anti-metamorphic and vitellogenic functions in insects via phosphorylation-mediated recruitment of specific cofactors
Background
The zinc-finger transcription factor Krüppel-homolog 1 (Kr-h1) exerts a dual regulatory role during insect development by preventing precocious larval/nymphal metamorphosis and in stimulating aspects of adult reproduction such as vitellogenesis. However, how Kr-h1 functions both as a transcriptional repressor in juvenile metamorphosis and an activator in adult reproduction remains elusive. Here, we use the insect
Locusta migratoria
to dissect the molecular mechanism by which Kr-h1 functions as activator and repressor at these distinct developmental stages.
Results
We report that the kinase PKCα triggers Kr-h1 phosphorylation at the amino acid residue Ser
154
, a step essential for its dual functions. During juvenile stage, phosphorylated Kr-h1 recruits a corepressor, C-terminal binding protein (CtBP). The complex of phosphorylated Kr-h1 and CtBP represses the transcription of
Ecdysone induced protein 93F
(
E93
) and consequently prevents the juvenile-to-adult transition. In adult insects, phosphorylated Kr-h1 recruits a coactivator, CREB-binding protein (CBP), and promotes vitellogenesis by inducing the expression of
Ribosomal protein L36
. Furthermore, Kr-h1 phosphorylation with the concomitant inhibition of
E93
transcription is evolutionarily conserved across insect orders.
Conclusion
Our results suggest that Kr-h1 phosphorylation is indispensable for the recruitment of transcriptional cofactors, and for its anti-metamorphic and vitellogenic actions in insects. Our data shed new light on the understanding of Kr-h1 regulation and function in JH-regulated insect metamorphosis and reproduction.
Journal Article
Regulatory mechanisms underlying the specification of the pupal-homologous stage in a hemimetabolous insect
Juvenile hormones and the genetic interaction between the transcription factors Krüppel homologue 1 ( Kr-h1 ) and Broad ( Br ) regulate the transformation of insects from immature to adult forms in both types of metamorphosis (holometaboly with a pupal stage versus hemimetaboly with no pupal stage); however, knowledge about the exact instar in which this occurs is limited. Using the hemimetabolous cricket Gryllus bimaculatus ( Gb ), we demonstrate that a genetic interaction occurs among Gb ′ Kr-h1 , Gb ′ Br and the adult-specifier transcription factor Gb ′ E93 from the sixth to final (eighth) nymphal instar. Gb ′ Kr-h1 and Gb ′ Br mRNAs were strongly expressed in the abdominal tissues of sixth instar nymphs, with precocious adult moults being induced by Gb ′ Kr-h1 or Gb ′ Br knockdown in the sixth instar. The depletion of Gb ′ Kr-h1 or Gb ′ Br upregulates Gb ′ E93 in the sixth instar. By contrast, Gb ′ E93 knockdown at the sixth instar prevents nymphs transitioning to adults, instead producing supernumerary nymphs. Gb ′ E93 also represses Gb ′ Kr-h1 and Gb ′ Br expression in the penultimate nymphal instar, demonstrating its important role in adult differentiation. Our results suggest that the regulatory mechanisms underlying the pupal transition in holometabolous insects are evolutionarily conserved in hemimetabolous G . bimaculatus , with the penultimate and final nymphal periods being equivalent to the pupal stage. This article is part of the theme issue ‘The evolution of complete metamorphosis’.
Journal Article
The innovation of the final moult and the origin of insect metamorphosis
The three modes of insect postembryonic development are ametaboly, hemimetaboly and holometaboly, the latter being considered the only significant metamorphosis mode. However, the emergence of hemimetaboly, with the genuine innovation of the final moult, represents the origin of insect metamorphosis and a necessary step in the evolution of holometaboly. Hemimetaboly derives from ametaboly and might have appeared as a consequence of wing emergence in Pterygota, in the early Devonian. In extant insects, the final moult is mainly achieved through the degeneration of the prothoracic gland (PG), after the formation of the winged and reproductively competent adult stage. Metamorphosis, including the formation of the mature wings and the degeneration of the PG, is regulated by the MEKRE93 pathway, through which juvenile hormone precludes the adult morphogenesis by repressing the expression of transcription factor E93, which triggers this change. The MEKRE93 pathway appears conserved in extant metamorphosing insects, which suggest that this pathway was operative in the Pterygota last common ancestor. We propose that the final moult, and the consequent hemimetabolan metamorphosis, is a monophyletic innovation and that the role of E93 as a promoter of wing formation and the degeneration of the PG was mechanistically crucial for their emergence. This article is part of the theme issue ‘The evolution of complete metamorphosis’.
Journal Article
Juvenile hormone resistance gene Methoprene-tolerant controls entry into metamorphosis in the beetle Tribolium castaneum
Besides being a spectacular developmental process, metamorphosis is key to insect success. Entry into metamorphosis is controlled by juvenile hormone (JH). In larvae, JH prevents pupal and adult morphogenesis, thus keeping the insect in its immature state. How JH signals to preclude metamorphosis is poorly understood, and a JH receptor remains unknown. One candidate for the JH receptor role is the Methoprene-tolerant (Met) Per-Arnt-Sim (PAS) domain protein [also called Resistance to JH, Rst (1)JH], whose loss confers tolerance to JH and its mimic methoprene in the fruit fly Drosophila melanogaster. However, Met deficiency does not affect the larval-pupal transition, possibly because this process does not require JH absence in DROSOPHILA: By contrast, the red flour beetle Tribolium castaneum is sensitive to developmental regulation by JH, thus making an ideal system to examine the role of Met in the antimetamorphic JH action. Here we show that impaired function of the Met ortholog TcMet renders Tribolium resistant to the effects of ectopic JH and, in a striking contrast to Drosophila, causes early-stage beetle larvae to undergo precocious metamorphosis. This is evident as TcMet-deficient larvae pupate prematurely or develop specific heterochronic phenotypes such as pupal-like cuticular structures, appendages, and compound eyes. Our results demonstrate that TcMet functions in JH response and provide the critical evidence that the putative JH receptor Met mediates the antimetamorphic effect of JH.
Journal Article