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Gut Development (gut + development)
Selected AbstractsDevelopment of the endoderm and gut in medaka, Oryzias latipesDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 5 2006Daisuke Kobayashi We performed an extensive analysis of endodermal development and gut tube morphogenesis in the medaka embryo by histology and in situ hybridization. The markers used in these analyses included sox17, sox32, foxA2, gata-4, -5, -6 and shh. sox17, sox32, foxA2, and gata-5 and -6 are expressed in the early endoderm to the onset of gut tube formation. Sections of medaka embryos hybridized with foxA2, a pan-endodermal marker during gut morphogenesis, demonstrated that gut tube formation is initiated in the anterior portion and that the anterior and mid/posterior gut undergo distinct morphogenetic processes. Tube formation in the anterior endoderm that is fated to the pharynx and esophagus is much delayed and appears to be independent of gut morphogenesis. The overall aspects of medaka gut development are similar to those of zebrafish, except that zebrafish tube formation initiates at both the anterior and posterior portions. Our results therefore describe both molecular and morphological aspects of medaka digestive system development that will be necessary for the characterization of medaka mutants. [source] Gli3 null mice display glandular overgrowth of the developing stomachDEVELOPMENTAL DYNAMICS, Issue 4 2005Jae H. Kim Abstract The role of the Hedgehog signaling pathway in various aspects of gut development is still poorly understood. In the developing stomach, Sonic (Shh) and Indian (Ihh) hedgehog are expressed in both distinct and overlapping regions. Loss of Sonic hedgehog function in the stomach results in a glandular phenotype of intestinal transformation and overgrowth. These changes are reminiscent of the pre-malignant lesion, intestinal metaplasia. To determine the role of Hedgehog-related transcription factors, Gli2 and Gli3, in Shh signaling during stomach development, we conducted a mutant analysis of glandular stomach from Shh, Gli2, and Gli3 mutant mice. Although Gli2 principally mediates the activator function of Shh, surprisingly we observed minimal changes in glandular development in the Gli2 mutant stomach. Furthermore, Gli3, which typically functions as a repressor of Hedgehog signal, showed a striking phenocopy of the glandular expansion and intestinal transformation found in Shh mutant stomach. A reduction in apoptotic events was seen in all mutant stomachs with no appreciable changes in proliferation. Both Shh and Gli3 mutant stomachs displayed early changes of intestinal transformation but these did not impact on the overall differentiation of the gastric epithelium. Interestingly, the observation that Gli3 shares a similar glandular phenotype to Shh mutant stomach reveals a possible novel role of Gli3 activator in the developing stomach. The embryonic stomach is a unique model of the Hedgehog pathway function and one that may help to uncover some of the mechanisms underlying the development of intestinal metaplasia. Developmental Dynamics 234:984,991, 2005. © 2005 Wiley-Liss, Inc. [source] Molecular mechanisms of early gut organogenesis: A primer on development of the digestive tractDEVELOPMENTAL DYNAMICS, Issue 2 2003Julie C. Kiefer Abstract Creating an organ poses unique challenges in embryogenesis, including establishing an organ primordium and coordinating development of different tissues in the organ. The digestive tract (gut) is a complex organ system, posing the interesting question of how the development of a series of organs is coordinated to establish an organ system with a common function. Although gut development has been the focus of much research, the molecular mechanisms that regulate these events are just beginning to be understood. This primer will first outline the basic anatomy of the digestive tract and then focus on molecular mechanisms that drive vertebrate gut organogenesis. Deciphering mechanisms underlying gut organogenesis also provides insights into understanding the development of other organs. Developmental Dynamics 228:287,291, 2003. © 2003 Wiley-Liss, Inc. [source] Novel regulation of yolk utilization by thyroid hormone in embryos of the direct developing frog Eleutherodactylus coquiEVOLUTION AND DEVELOPMENT, Issue 5 2010Srikanth Singamsetty SUMMARY Thyroid hormone (TH) is required for metamorphosis of the long, coiled tadpole gut into the short frog gut. Eleutherodactylus coqui, a direct developing frog, lacks a tadpole. Its embryonic gut is a miniature adult form with a mass of yolky cells, called nutritional endoderm, attached to the small intestine. We tested the TH requirement for gut development in E. coqui. Inhibition of TH synthesis with methimazole arrested gut development in its embryonic form. Embryos treated with methimazole failed to utilize the yolk in their nutritional endoderm, and survived for weeks without further development. Conversely, methimazole and 3,3,,5-tri-iodo- l -thyronine, the active form of TH, stimulated gut development and utilization and disappearance of the nutritional endoderm. In Xenopus laevis, the receptor for TH, TR,, is upregulated in response to TH. Similarly, EcTR,, the E. coqui ortholog, was upregulated by TH in the gut. EcTR, expression was high in the nutritional endoderm, suggesting a direct role for TH in yolk utilization by these cells. An initial step in the breakdown of yolk in X. laevis is acidification of the yolk platelet. E. coqui embryos in methimazole failed to acidify their yolk platelets, but acidification was stimulated by TH indicating its role in an early step of yolk utilization. In addition to a conserved TH role in gut development, a novel regulatory role for TH in yolk utilization has evolved in these direct developers. [source] Effect of Microparticulate Diets on Growth and Survival of Spotted Sand Bass Larvae, Paralabrax maculatofasciatus, at Two Early Weaning TimesJOURNAL OF THE WORLD AQUACULTURE SOCIETY, Issue 1 2008Roberto Civera-Cerecedo Early weaning in spotted sand bass larvae, Paralabrax maculatofasciatus, was evaluated, testing a combination of two weaning times, 17 and 22 d after hatching (d.a.h.), and three different microparticulate diets. Protein in diets was mainly from sardine meal and from 15% squid meal, beef blood meal, or fish protein hydrolysate. Anatomical (standard length), histological (gut development), and biochemical (highly unsaturated fatty acids) parameters were measured in larvae, as well as survival and resistance to a stress test measured 40 d.a.h. For larvae weaned at 17 d.a.h., the best growth and survival were obtained with diets containing fish protein hydrolysates; for larvae weaned at 22 d.a.h., best results were obtained with squid meal and fish protein hydrolysate. Growth and survival were significantly lower when using beef blood meal in both weaning treatments. The best relative and total survival were for larvae weaned at 22 d.a.h. After the resistance test, 100% survival occurred in larvae fed on any microparticulate diet and either weaning treatment. No significant differences in arachidonic acid, eicosapentaenoic acid, or docosahexaenoic acid concentrations in fish fed on any diet occurred. Results suggest that weaning at 22 d.a.h. with diets containing fish protein hydrolysate or squid meal is preferred by this species. [source] Evaluation of the NK2 Homeobox 1 Gene (NKX2-1) as a Hirschsprung's Disease Locus THIS ARTICLE HAS BEEN RETRACTEDANNALS OF HUMAN GENETICS, Issue 2 2008M.-M. Garcia-Barceló Summary Hirschsprung's disease (HSCR, colonic aganglionosis) is an oligogenic entity that usually requires mutations in RET and other interacting loci. Decreased levels of RET expression may lead to the manifestation of HSCR. We previously showed that RET transcription was decreased due to alteration of the NKX2,1 binding site by two HSCR-associated RET promoter single nucleotide polymorphisms (SNPs). This prompted us to investigate whether DNA alterations in NKX2-1 could play a role in HSCR by affecting the RET -regulatory properties of the NKX2,1 protein. Our initial study on 86 Chinese HSCR patients revealed a Gly322Ser amino acid substitution in the NKX2,1 protein. In this study, we have examined 102 additional Chinese and 70 Caucasian patients and 194 Chinese and 60 Caucasian unselected, unrelated, subjects as controls. The relevance of the DNA changes detected in NKX2-1 by direct sequencing were evaluated using bioinformatics, reporter and binding-assays, mouse neurosphere culture, immunohistochemistry and immunofluorescence techniques. Met3Leu and Pro48Pro were identified in 2 Caucasian and 1 Chinese patients respectively. In vitro analysis showed that Met3Leu reduced the activity of the RET promoter by 100% in the presence of the wild-type or HSCR-associated RET promoter SNP alleles. The apparent binding affinity of the NKX2,1 mutated protein was not decreased. The Met3Leu mutation may affect the interaction of NKX2,1 with its protein partners. The absence of NKX2-1 expression in mouse but not in human gut suggests that the role of NKX2,1 in gut development differs between the two species. NKX2-1 mutations could contribute to HSCR by affecting RET expression through defective interactions with other transcription factors. [source] Left-right asymmetry in gut development: what happens next?BIOESSAYS, Issue 10 2009Sally F Burn The gastrointestinal tract is an asymmetrically patterned organ system. The signals which initiate left-right asymmetry in the developing embryo have been extensively studied, but the downstream steps required to confer asymmetric morphogenesis on the gut organ primordia are less well understood. In this paper we outline key findings on the tissue mechanics underlying gut asymmetry, across a range of species, and use these to synthesise a conserved model for asymmetric gut morphogenesis. We also discuss the importance of correct establishment of left-right asymmetry for gut development and the consequences of perturbations in this process. [source] | ||||||||||