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The essential role of bursicon during Drosophila development
Brandon J Loveall, David L Deitcher
BMC Developmental Biology , 2010, DOI: 10.1186/1471-213x-10-92
Abstract: We addressed the mechanism and timing of hormonal release from bursicon-positive motor neurons at the larval neuromuscular junction. Our findings indicate that vesicle membrane proteins which are required for classical neurotransmitter release are also expressed at these peptidergic motor neuron terminals; and that these terminals secrete hormones including bursicon at the neuromuscular junction, coinciding with larval ecdysis. This release surprisingly occurs in two waves, indicating bursicon secretion preceding and following the ecdysis sequence. Next, we addressed the functional significance of bursicon signaling during development, by disrupting the expression of its receptor, rickets, in different target tissues. We determined that rickets is developmentally required in the epidermis and imaginal discs for proper formation of the prepupa. It is also required to harden the pharate adult cuticle before eclosion. Significantly, we have also found that the available rickets mutants are not genetic nulls as previously believed, which necessitated the use of targeted RNA interference to disrupt rickets expression.Our results are consistent with the view that bursicon is the insect tanning hormone. However, this is the first study to rigorously demonstrate both its release and function during development. Importantly, we provide new evidence that bursicon release can precede the initiation of larval ecdysis, and that bursicon tans the puparium. Our results firmly establish bursicon signaling as essential to insect growth and development.For all their remarkable diversity, all insects are faced with a recurring problem during their development: the replacement of a constricting exoskeleton after periods of intermolt growth. The successful solution to this problem is to form a new, larger cuticle beneath the hardened exoskeleton. Shedding of the older exoskeleton can only occur once the new cuticle is complete. The cuticle-shedding behaviors collectively known as ecdysi
Global identification of bursicon-regulated genes in Drosophila melanogaster
Shiheng An, Songjie Wang, Lawrence I Gilbert, Brenda Beerntsen, Mark Ellersieck, Qisheng Song
BMC Genomics , 2008, DOI: 10.1186/1471-2164-9-424
Abstract: We used DNA microarray analysis to identify bursicon-regulated genes in neck-ligated flies (Drosophila melanogaster) that received recombinant bursicon (r-bursicon). Fifty four genes were found to be regulated by bursicon 1 h post r-bursicon injection, 52 being up-regulated and 2 down-regulated while 33 genes were influenced by r-bursicon 3 h post-injection (24 up-regulated and 9 down-regulated genes). Analysis of these genes by inference from the fly database http://flybase.bio.indiana.edu webcite revealed that these genes encode proteins with diverse functions, including cell signaling, gene transcription, DNA/RNA binding, ion trafficking, proteolysis-peptidolysis, metabolism, cytoskeleton formation, immune response and cell-adhesion. Twenty eight genes randomly selected from the microarray-identified list were verified by real time PCR (qPCR) which supported the microarray data. Temporal response studies of 13 identified and verified genes by qPCR revealed that the temporal expression patterns of these genes are consistent with the microarray data.Using r-bursicon, we identified 87 genes that are regulated by bursicon, 30 of which have no previously known function. Most importantly, all genes randomly selected from the microarray-identified list were verified by real time PCR. Temporal analysis of 13 verified genes revealed that the expression of these genes was indeed induced by bursicon and correlated well with the cuticle sclerotization process. The composite data suggest that these genes play important roles in regulating the cuticle sclerotization and wing expansion processes. The data obtained here will form the basis for future studies aimed at elucidating the exact mechanisms upstream from the secretion of bursicon and its binding to target cells.Molting is a process common to all arthropods, during which a larger new cuticle is synthesized and the old one is digested and cast off (ecdysis) allowing the animal to grow. Studies on ecdysial behavior in inse
Insect Neuropeptide Bursicon Homodimers Induce Innate Immune and Stress Genes during Molting by Activating the NF-κB Transcription Factor Relish  [PDF]
Shiheng An, Shengzhang Dong, Qian Wang, Sheng Li, Lawrence I. Gilbert, David Stanley, Qisheng Song
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034510
Abstract: Background Bursicon is a heterodimer neuropeptide composed of two cystine knot proteins, bursicon α (burs α) and bursicon β (burs β), that elicits cuticle tanning (melanization and sclerotization) through the Drosophila leucine-rich repeats-containing G protein-coupled receptor 2 (DLGR2). Recent studies show that both bursicon subunits also form homodimers. However, biological functions of the homodimers have remained unknown until now. Methodology/Principal Findings In this report, we show in Drosophila melanogaster that both bursicon homodimers induced expression of genes encoding antimicrobial peptides (AMPs) in neck-ligated adults following recombinant homodimer injection and in larvae fat body after incubation with recombinant homodimers. These AMP genes were also up-regulated in 24 h old unligated flies (when the endogenous bursicon level is low) after injection of recombinant homodimers. Up-regulation of AMP genes by the homodimers was accompanied by reduced bacterial populations in fly assay preparations. The induction of AMP expression is via activation of the NF-κB transcription factor Relish in the immune deficiency (Imd) pathway. The influence of bursicon homodimers on immune function does not appear to act through the heterodimer receptor DLGR2, i.e. novel receptors exist for the homodimers. Conclusions/Significance Our results reveal a mechanism of CNS-regulated prophylactic innate immunity during molting via induced expression of genes encoding AMPs and genes of the Turandot family. Turandot genes are also up-regulated by a broader range of extreme insults. From these data we infer that CNS-generated bursicon homodimers mediate innate prophylactic immunity to both stress and infection during the vulnerable molting cycle.
Familial hypophosphatemic rickets  [cached]
Sattur A,Naikmasur V,Shrivastava R,Babshet M
Journal of the Indian Society of Pedodontics and Preventive Dentistry , 2010,
Abstract: Rickets is the failure of mineralization of osteoid and newly formed bones in a child skeleton. It is commonly associated with vitamin D deficiency; however, it can be because of a decrease in the serum phosphate levels leading to inadequate mineralization of cartilage and bone, consequent skeletal deformities, and growth retardation. The hypophosphatemic conditions that interfere in bone mineralization comprise many hereditary or acquired diseases. One of the hereditary types of hypophosphatemic rickets is the familial hypophosphatemic rickets. This rare variety was diagnosed in a 9-year-old patient who had come with a chief complaint of a missing tooth. In the present case, radiographic aspects of oral and systemic manifestations of familial hypophosphatemic rickets are highlighted.
"Hypercalciuric hypophosphatemic rickets "
Karamifar H,Amirhakimi GH
Acta Medica Iranica , 2001,
Abstract: A 13 year- old girl had rickets clinically evident sicne she was 10 years of age. She received multiple doses of vitamin D3 without improvement.This patient manifested an unusal form of hypophosphatemic rickets with hypercalciuria. It is recommended that urinary calcium excretion be assessed in all patients with hypophosphatemic rickets before the initiation of any therapy
Epidermolytic hyperkeratosis with rickets
Nayak Surajit,Behera Samira,Acharjya Basanti,Sahu A
Indian Journal of Dermatology, Venereology and Leprology , 2006,
Abstract: A 6-year-old child presented with generalized hyperkeratosis, most marked over the flexures; windswept deformity of the legs; and limping since 3 years. On the basis of the clinical, histopathologic and biochemical findings, he was diagnosed as a case of epidermolytic hyperkeratosis with rickets. He was treated with parenteral vitamin D3 and calcium supplements orally. Nutritional rickets has been reported in children with various types of ichthyosis like lamellar and X-linked types. We report this case of epidermolytic hyperkeratosis with rickets for its rarity.
Incidental Rickets in the Emergency Department Setting
John V. Zurlo,Shaun R. Wagner
Case Reports in Medicine , 2012, DOI: 10.1155/2012/163289
Abstract: Vitamin D deficiency rickets is a childhood osteomalacia, with impaired skeletal development and potentially skeletal deformities. The radiographic findings of rickets are many but include widening, fraying, and cupping of the metaphysis. Developmental delay and related complications of seizure and tetany have also been reported. This medical entity is often thought of as a classic medical disease of the past. However, it persists, and the recognition of rickets is on the rise. The reemergence of rickets correlates with the increase in the number of children exclusively breastfed and with the frequent use of sun block in the pediatric population. We present two cases of rickets, diagnosed through a visit to the Emergency Department made for unrelated symptoms. These two cases illustrate the importance of diagnosing rickets as an “incidental” finding. With early detection, dietary supplementation can be initiated potentially sparing the patient symptomatic disease.
Hypophosphatemic rickets and osteomalacia
Menezes Filho, Hamilton de;Castro, Luiz Claudio G. de;Damiani, Durval;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2006, DOI: 10.1590/S0004-27302006000400025
Abstract: the hypophosphatemic conditions that interfere in bone mineralization comprise many hereditary or acquired diseases, all of them sharing the same pathophysiologic mechanism: reduction in the phosphate reabsorption by the renal tubuli. this process leads to chronic hyperphosphaturia and hypophosphatemia, associated with inappropriately normal or low levels of calcitriol, causing osteomalacia or rickets in children and osteomalacia in adults. x-linked hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, and tumor-induced osteomalacia are the main syndromes involved in the hypophosphatemic rickets. although these conditions exhibit different etiologies, there is a common link among them: increased activity of a phosphaturic factor, being the fibroblast growth factor 23 (fgf-23) the most studied one and to which is attributed a central role in the pathophysiology of the hyperphosphaturic disturbances. activating mutations of fgf-23 and inactivating mutations in the phex gene (a gene on the x chromosome that codes for a zn-metaloendopeptidase proteolytic enzyme which regulates the phosphate) involved in the regulation of fgf-23 have been identified and have been implicated in the pathogenesis of these disturbances. genetic studies tend to show that the phosphorus homeostasis depends on a complex osteo-renal metabolic axis, whose mechanisms of interaction have been poorly understood so far. this paper reviews the current knowledge status concerning the pathophysiology of phosphate metabolism regulation and the pathophysiologic basis of hypophosphatemic rickets. it also analyzes the clinical picture and the therapeutic aspects of these conditions as well.
A Retrospective Evaluation of Patients with Rickets
Muzaffer Ocak,Erdal Eren,Kenan ?stanbullu,Halil Sa?lam
Güncel Pediatri , 2011,
Abstract: Introduction: Rickets is a group of diseases presenting with skeletal deformities and decreased growth rate due to diminished epiphyseal calcification. It has been previously reported that in our country, nutritional rickets with Vitamin D insufficiency is an important healthcare problem.Material and Method: In this study, we have evaluated 20 patients with rickets being followed up in pediatric endocrinology outpatient clinic of Uludag University between 2006 and 2010. The diagnosis of nutritional rickets was defined with positive response to treatment and hypocalcaemia accompanied by one of the followings; rickets specific radiological changes, high alkaline phosphates levels or low Vitamin D levels. p<0.05 is accepted as statistically significant. The statistical analysis was performed using SPSS 16.0.Results: A total of 14 boys and 6 girls were included in this study. Ten of the patients were considered as nutritional rickets, 5 were hypophosphatemic rickets and 5 were vitamin D dependent rickets type 1. On radiological evaluation, distal metaphyseal enlargement-irregularity of radius and ulna was found in 11 patients. O-bain deformity was seen in 3 patients. Ten of the patients were from small districts, 5 were from villages and the remainders were from city center. The main complaints were short stature in 5 patients, difficulty in walking in 4 patients, recurrent pneumonia in 4 patients, seizure in 4 patients, bone deformity in 3 patients, tetany in 2 patients, and ballismus in one patient. Discussion: Rickets is still a major health problem in childhood. It must be kept in mind in the patients who have short stature and difficulty in walking. Vitamin D dependent rickets or hypophosphatemic rickets must be considered in the patients who have signs and symptoms of rickets in spite of regular vitamin D supplementation. These patients should be referred to a pediatric endocrinologist. (Jo-ur-nal of Cur-rent Pe-di-at-rics 2011; 9: 75-8)
Epidemiology of nutritional rickets in children  [cached]
Al-Atawi M,Al-Alwan I,Al-Mutair A,Tamim H
Saudi Journal of Kidney Diseases and Transplantation , 2009,
Abstract: In most developing countries, nutritional rickets is a major health problem. The aim of this study was to explore the magnitude of nutritional rickets among Saudi infants, and the various clinical presentations, as well as to address the possible operating risk factors behind the disease. We carried out a retrospective study at King Abdulaziz Medical City-King Fahad National Guard Hospital in Riyadh, Saudi Arabia. The records of Saudi infants under the age of 14 months over a 10-year period (between January 1990 and January 2000) were reviewed. Infor-mation collected included age, sex, clinical presentations, biochemical, radiological findings, infant nutrition, presence of other nutritional deficiencies and exposure to sunlight. There were 283 infants diagnosed with nutritional rickets due to Vitamin D deficiency (67% males) who were between 6 and 14 months of age. Among the total, 70% were exclusively breast-fed, and 23% were breast-fed until the age of 1 year. The most frequent clinical presentation was hypo-calcemic convulsions (34%) followed by chest infections (33%) and gastroenteritis (25%). In conclusion, nutritional rickets is still prevalent in Saudi Arabia with the primary etiology being vitamin D deficiency. Therefore we recommend that every infant, who is exclusively on breast-feeding, has routine supplement of vitamin D in the range of 200 IU/day (alone or as apart of multivitamin), started soon after birth until the time of weaning.
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