Prothoracicotropic hormone modulates environmental adaptive plasticity through the control of developmental timing (original) (raw)
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Prothoracicotropic Hormone Regulates Developmental Timing and Body Size in Drosophila
Developmental Cell, 2007
In insects, control of body size is intimately linked to nutritional quality as well as environmental and genetic cues that regulate the timing of developmental transitions. Prothoracicotropic hormone (PTTH) has been proposed to play an essential role in regulating the production and/or release of ecdysone, a steroid hormone that stimulates molting and metamorphosis. In this report we examine the consequences on Drosophila development of ablating the PTTH-producing neurons. Surprisingly, PTTH production is not essential for molting or metamorphosis. Instead, loss of PTTH results in delayed larval development and eclosion of larger flies with more cells. Prolonged feeding, without changing the rate of growth, causes the developmental delay and is a consequence of low ecdysteroid titers. These results indicate that final body size in insects is determined by a balance between growth rate regulators such as insulin and developmental timing cues such as PTTH that set the duration of the feeding interval.
Endocrine regulation of predator-induced phenotypic plasticity
Oecologia, 2014
Elucidating the developmental and genetic control of phenotypic plasticity remains a central agenda in evolutionary ecology. Here, we investigate the physiological regulation of phenotypic plasticity induced by another organism, specifically predator-induced phenotypic plasticity in the model ecological and evolutionary organism Daphnia pulex. Our research centres on using molecular tools to test among alternative mechanisms of developmental control tied to hormone titres, receptors and their timing in the life cycle. First, we synthesize detail about predator-induced defenses and the physiological regulation of arthropod somatic growth and morphology, leading to a clear prediction that morphological defences are regulated by juvenile hormone and life-history plasticity by ecdysone and juvenile hormone. We then show how a small network of genes can differentiate phenotype expression between the two primary developmental control pathways in arthropods: juvenoid and ecdysteroid hormon...
Peptides, 2014
The paradigm saying that release of the brain neuropeptide big prothoracicotropic hormone (PTTH) initiates metamorphosis by activating the Torso-receptor/ERK pathway in larval prothoracic glands (PGs) is widely accepted nowadays. Upon ligand-receptor interaction Ca(2+) enters the PG cells and acts as a secondary messenger. Ecdysteroidogenesis results, later followed by apoptosis. Yet, some data do not fit in this model. In some species decapitated animals can still molt, even repeatedly, and metamorphose. PTTH does not universally occur in all insect species. PGs may also have other functions; PGs as counterpart of the vertebrate thymus? There are also small PTTHs. Finally, PTTH remains abundantly present in adults and plays a role in control of ecdysteroidogenesis (=sex steroid production) in gonads. This is currently documented only in males. This urges a rethinking of the PTTH-PG paradigm. The key question is: Why does PTTH-induced Ca(2+) entry only result in ecdysteroidogenesis ...
Journal of Insect Physiology, 1992
The role of the brain as a. neuroendocrine regulator of metamorphosis in the gypsy moth, Lymantria dispar L. was originally demonstrated by Kopec more than 70 years ago. We have reexamined this role by determining haemolymph ecdysteroid titres, activity and responsiveness of the prothoracic glands, and growth of female last (i.e. fifth)-instar larvae in relation to secretion of the brain prothoracicotropic hormone (PTTH), the factor known to trigger moulting and metamorphosis in insects. The head critical period for secretion of PTTH in Lymantria reared at 25°C in a 16 h light-8 h dark cycle was shown by neck ligation to occur on day 7-8 of the fifth instar. The critical period occurred shortly after a small peak of haemolymph ecdysteroid that reached 600 pg 20-hydroxyecdysone equivalents/PI, as determined by radioimmunoassay. Feeding was completed by day 7, thus neck ligation did not affect nutrient intake. Animals starved from day 5 onward completed pupation at the same time as non-starved controls and showed normal increases in haemolymph ecdysteroid titres. Animals neck-ligated on day 7 and injected 5 days later with extracts of brain, retrocerebral complex, or brain tissues containing lateral or median neurosecretory cells were stimulated to pupate within 5 days, and brain-extract-injected animals showed an increase in haemolymph ecdysteroid titre of over 4000 pg/pl. Animals neck-ligated earlier had lower haemolymph ecdysteroid titres than day 7, neck-ligated larvae and their prothoracic glands showed lower activity in vitro. Using the in vivo assay, PTTH activity was detected in pre-hatch eggs and in brains taken from day-5 last-instar larvae, day-l pupae and day-l adults. The assay appears specific to tissues from the brain and retrocerebral complex, since no activity was found with extracts of the subesophageal ganglion, fat body or muscle.
Importance of juvenile hormone signaling arises with competence of insect larvae to metamorphose
Developmental Biology, 2014
Juvenile hormone (JH) postpones metamorphosis of insect larvae until they have attained an appropriate stage and size. Then, during the final larval instar, a drop in JH secretion permits a metamorphic molt that transforms larvae to adults either directly (hemimetaboly) or via a pupal stage (holometaboly). In both scenarios, JH precludes metamorphosis by activating the Kr-h1 gene through a JH receptor, Methoprene-tolerant (Met). Removal of Met, Kr-h1, or JH itself triggers deleterious precocious metamorphosis. Although JH is thought to maintain the juvenile status throughout larval life, various methods of depleting JH failed to induce metamorphosis in early-instar larvae. To determine when does JH signaling become important for the prevention of precocious metamorphosis, we chose the hemimetabolous bug, Pyrrhocoris apterus, and the holometabolous silkworm, Bombyx mori. Both species undergo a fixed number of five larval instars. Pyrrhocoris larvae subjected to RNAi-mediated knockdown of Met or Kr-h1 underwent precocious adult development when treated during the fourth (penultimate) instar, but younger larvae proved increasingly resistant to loss of either gene. The earliest instar developing minor signs of precocious metamorphosis was the third. Therefore, the JH-response genes may not be required to maintain the larval program during the first two larval instars. Next, we examined Bombyx mod mutants that cannot synthesize authentic, epoxidized forms of JH. Although mod larvae expressed Kr-h1 mRNA at severely reduced levels since hatching, they only entered metamorphosis by pupating after four, rarely three instars. Based on findings in Pyrrhocoris and Bombyx, we propose that insect postembryonic development is initially independent of JH. Only later, when larvae gain competence to enter metamorphosis, JH signaling becomes necessary to prevent precocious metamorphosis and to optimize growth.
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 2012
Prothoracicotropic hormone (PTTH) is a brain neurohormone that has been studied for over 80 years. The only known target of PTTH is the prothoracic glands (PGs) of larvae, which synthesize the insect molting hormones (ecdysteroids) and a massive literature exists on this axis. The PGs degenerate around the time of adult emergence, yet presence of PTTH has been reported in the brains of several adult insects. Using an in vitro bioassay system, we confirm that PTTH is present in the adult female brain of Rhodnius prolixus. The material is electrophoretically, immunologically and biologically indistinguishable from larval PTTH. The amount of PTTH in the brain shows a daily rhythm during egg development. We show that brains in vitro release PTTH with a daily rhythm over this period of time. PTTH is released at each scotophase. This is the first report that PTTH is released from the adult brain and functions as a hormone, inviting explanation of its function. Larval PTTH is also known to be released with a daily rhythm, and the clock in the brain controls both larval and adult rhythms. The potential significance of rhythmic PTTH release in female adults is discussed in relation to the regulation of ecdysteroids, egg development and the concept of internal temporal order.
Specific transcriptional responses to juvenile hormone and ecdysone in Drosophila
Insect Biochemistry and Molecular Biology, 2007
Previous studies have shown that ecdysone (E), and its immediate downstream product 20-hydroxyecdysone (20E), can have different biological functions in insects, suggesting that E acts as a distinct hormone. Here, we use Drosophila larval organ culture in combination with microarray technology to identify genes that are transcriptionally regulated by E, but which show little or no response to 20E. These genes are coordinately expressed for a brief temporal interval at the onset of metamorphosis, suggesting that E acts together with 20E to direct puparium formation. We also show that E74B, pepck, and CG14949 can be induced by juvenile hormone III (JH III) in organ culture, and that CG14949 can be induced by JH independently of protein synthesis. In contrast, E74A and E75A show no response to JH in this system. These studies demonstrate that larval organ culture can be used to identify Drosophila genes that are regulated by hormones other than 20E, and provide a basis for studying crosstalk between multiple hormone signaling pathways. r