A juvenile hormone agonist reveals distinct developmental pathways mediated by Ecdysone-inducible broad complex transcription factors

Restifo, Linda L.; Wilson, Thomas G.

doi:10.1002/(sici)1520-6408(1998)22:2<141::aid-dvg4>3.0.co;2-6

Cited by 94 publications

(71 citation statements)

References 98 publications

(135 reference statements)

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“…Our knowledge about the molecular events underlying metamorphosis is primarily based on the Drosophila model. Unfortunately, fly development has largely lost dependence on JH, as constant exposure to JH cannot prevent entry to the pupal program (Riddiford and Ashburner, 1991;Restifo and Wilson, 1998). Thus, in response to an elevated ecdysteroid titer, Drosophila larval epidermis dies and the adult head and thorax, with appendages, develop from imaginal discs, while the abdominal epidermis proliferates from histoblasts (Madhavan and Schneiderman, 1977;Bayer et al, 1996b).…”

Section: Introductionmentioning

confidence: 89%

Broad-Complex acts downstream of Met in juvenile hormone signaling to coordinate primitive holometabolan metamorphosis

2008

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Metamorphosis of holometabolous insects, an elaborate change of form between larval, pupal and adult stages, offers an ideal system to study the regulation of morphogenetic processes by hormonal signals. Metamorphosis involves growth and differentiation, tissue remodeling and death, all of which are orchestrated by the morphogenesis-promoting ecdysteroids and the antagonistically acting juvenile hormone (JH), whose presence precludes the metamorphic changes. How target tissues interpret this combinatorial effect of the two hormonal cues is poorly understood, mainly because JH does not prevent larval-pupal transformation in the derived Drosophila model, and because the JH receptor is unknown. We have recently used the red flour beetle Tribolium castaneum to show that JH controls entry to metamorphosis via its putative receptor Methoprene-tolerant (Met). Here, we demonstrate that Met mediates JH effects on the expression of the ecdysteroid-response gene Broad-Complex (BR-C). Using RNAi and a classical mutant, we show that Tribolium BR-C is necessary for differentiation of pupal characters. Furthermore, heterochronic combinations of retarded and accelerated phenotypes caused by impaired BR-C function suggest that besides specifying the pupal fate, BR-C operates as a temporal coordinator of hormonally regulated morphogenetic events across epidermal tissues. Similar results were also obtained when using the lacewing Chrysopa perla (Neuroptera), a member of another holometabolous group with a primitive type of metamorphosis. The tissue coordination role of BR-C may therefore be a part of the Holometabola groundplan.

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Section: Introductionmentioning

confidence: 89%

Broad-Complex acts downstream of Met in juvenile hormone signaling to coordinate primitive holometabolan metamorphosis

2008

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“…Although application of a JH mimic at metamorphosis is known to disrupt the gross anatomy of the nervous system in Drosophila (Restifo and Wilson, 1998), its effect on the growth of single identified neurons has not been reported previously. Knowing that JH is absent during the pupal-adult transition (Riddiford, 1993), we applied JHm to prepupae and pupae to explore how it would alter the growth of the arbor of ddaE.…”

Section: Application Of Juvenile Hormone Mimic During Metamorphosis Mmentioning

confidence: 99%

Mechanisms of Dendritic Elaboration of Sensory Neurons inDrosophila: Insights fromIn VivoTime Lapse

Williams¹,

Truman²

2004

J. Neurosci.

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In vivo time-lapse multiphoton microscopy was used to analyze the remodeling of the dendritic arborizing (da) sensory neuron known as dorsal dendritic arborizing neuron E (ddaE) during metamorphosis. After its larval processes have been removed, the cell body of ddaE repositions itself on the body wall between 25 and 40 hr after puparium formation (APF) and begins its adult outgrowth at 40 hr APF. The scaffold of the arbor is laid down between 40 and 54 hr APF, when growth is characterized by high filopodial activity at both terminal and interstitial positions and by branch retraction along with branch establishment. Later in development, filopodial activity remains high but is confined to terminal branches, and branch retraction is no longer seen. Treatment with the insect hormone juvenile hormone (JH), a key regulator of metamorphosis, alters the shape and complexity of the adult dendritic tree in a time-dependent manner. Early treatments with juvenile hormone mimic (JHm) appear to repress extension programs and maintain retraction programs. With later JHm treatments, extension programs appear normal, but retraction programs are maintained beyond their normal time. The JH treatments show the importance of retraction programs in establishing the overall arbor shape.

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“…Cloning and sequencing of the Met(+)-gene showed homology to the basic helix-loophelix-PAS family of transcription factors, implicating Met protein in a gene regulatory function of JH (20). Met(+) could now be linked to the ecdysone-inducible Broad-Complex transcription factors (21), suggesting that it is an early downstream element in the JH response cascade. Looking for gene products that interact with Met(+) may turn out to be an interesting alternative in the search strategies for the JH receptor.…”

Section: K Hartfeldermentioning

confidence: 99%

Insect juvenile hormone: from "status quo" to high society

Hartfelder

2000

Braz J Med Biol Res

260

165

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Juvenile hormone (JH) exerts pleiotropic functions during insect life cycles. The regulation of JH biosynthesis by neuropeptides and biogenic amines, as well as the transport of JH by specific binding proteins is now well understood. In contrast, comprehending its mode of action on target organs is still hampered by the difficulties in isolating specific receptors. In concert with ecdysteroids, JH orchestrates molting and metamorphosis, and its modulatory function in molting processes has gained it the attribute status quo hormone. Whereas the metamorphic role of JH appears to have been widely conserved, its role in reproduction has been subject to many modifications. In many species, JH stimulates vitellogenin synthesis and uptake. In mosquitoes, however, this function has been transferred to ecdysteroids, and JH primes the ecdysteroid response of developing follicles. As reproduction includes a variety of specific behaviors, including migration and diapause, JH has come to function as a master regulator in insect reproduction. The peak of pleiotropy was definitely reached in insects exhibiting facultative polymorphisms. In wingdimorphic crickets, differential activation of JH esterase determines wing length. The evolution of sociality in Isoptera and Hymenoptera has also extensively relied on JH. In primitively social wasps and bumble bees, JH integrates dominance position with reproductive status. In highly social insects, such as the honey bee, JH has lost its gonadotropic role and now regulates division of labor in the worker caste. Its metamorphic role has been extensively explored in the morphological differentiation of queens and workers, and in the generation of worker polymorphism, such as observed in ants.

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A juvenile hormone agonist reveals distinct developmental pathways mediated by Ecdysone-inducible broad complex transcription factors

Cited by 94 publications

References 98 publications

Broad-Complex acts downstream of Met in juvenile hormone signaling to coordinate primitive holometabolan metamorphosis

Broad-Complex acts downstream of Met in juvenile hormone signaling to coordinate primitive holometabolan metamorphosis

Mechanisms of Dendritic Elaboration of Sensory Neurons inDrosophila: Insights fromIn VivoTime Lapse

Insect juvenile hormone: from "status quo" to high society

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