Talk:Gastrointestinal Tract Development

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Cite this page: Hill, M.A. (2024, March 28) Embryology Gastrointestinal Tract Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Gastrointestinal_Tract_Development

10 Most Recent Papers

Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)


Gastrointestinal Tract Development

<pubmed limit=5>Gastrointestinal Tract Development</pubmed>


Historic Embryology: 1878 Alimentary Canal | 1882 The Organs of the Inner Germ-Layer The Alimentary Tube with its Appended Organs | 1902 The Organs of Digestion | 1907 Development of the Digestive System | 1907 Atlas | 1907 23 Somite Embryo | 1912 Digestive Tract | 1917 Entodermal Canal | 1918 Anatomy | 1921 Alimentary Tube


1902 Stomach | 1912 Stomach | 1921 Stomach

Papers

1891 26 Day Embryo


2014

Potential Regulatory Role of MicroRNAs in the Development of Bovine Gastrointestinal Tract during Early Life

PLoS One. 2014 Mar 28;9(3):e92592. doi: 10.1371/journal.pone.0092592. eCollection 2014.

Liang G1, Malmuthuge N1, McFadden TB2, Bao H1, Griebel PJ3, Stothard P1, Guan LL1. Author information

Abstract This study aimed to investigate the potential regulatory role of miRNAs in the development of gastrointestinal tract (GIT) during the early life of dairy calves. Rumen and small intestinal (mid-jejunum and ileum) tissue samples were collected from newborn (30 min after birth; n = 3), 7-day-old (n = 6), 21-day-old (n = 6), and 42-day-old (n = 6) dairy calves. The miRNA profiling was performed using Illumina RNA-sequencing and the temporal and regional differentially expressed miRNAs were further validated using qRT-PCR. Analysis of 16S rRNA gene copy numbers was used to quantify total bacteria, Bifidobacterium and Lactobacillus species. The expression of miR-143 was abundant in all three gut regions, at all time points and it targets genes involved primarily in the proliferation of connective tissue cells and muscle cells, suggesting a role in regulating rapid tissue development during the early life of calves. The expression of miR-146, miR-191, miR-33, miR-7, miR-99/100, miR-486, miR-145, miR-196 and miR-211 displayed significant temporal differences (FDR <0.05), while miR-192/215, miR-194, miR-196, miR-205 and miR-31 revealed significant regional differences (FDR <0.05). The expression levels of miR-15/16, miR-29 and miR-196 were positively correlated with the copy numbers of 16S rRNA gene of Bifidobacterium or Lactobacillus species or both (P<0.05). Functional analysis using Ingenuity Pathway Analysis identified the above mentioned differentially expressed miRNAs as potential regulators of gut tissue cell proliferation and differentiation. The bacterial density-associated miRNAs were identified as modulators of the development of lymphoid tissues (miR-196), maturation of dendritic cells (miR-29) and development of immune cells (miR-15/16). The present study revealed temporal and regional changes in miRNA expression and a correlation between miRNA expression and microbial population in the GIT during the early life, which provides further evidence for another mechanism by which host-microbial interactions play a role in regulating gut development.

PMID 24682221

2012

2011

Endodermal Hedgehog signals modulate Notch pathway activity in the developing digestive tract mesenchyme

Development. 2011 Aug;138(15):3225-33.

Kim TH, Kim BM, Mao J, Rowan S, Shivdasani RA. Source Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.

Abstract

The digestive tract epithelium and its adjoining mesenchyme undergo coordinated patterning and growth during development. The signals they exchange in the process are not fully characterized but include ligands of the Hedgehog (Hh) family, which originate in the epithelium and are necessary for mesenchymal cells to expand in number and drive elongation of the developing gut tube. The Notch signaling pathway has known requirements in fetal and adult intestinal epithelial progenitors. We detected Notch pathway activity in the embryonic gut mesenchyme and used conditional knockout mice to study its function. Selective disruption of the Notch effector gene RBP-Jκ (Rbpj) in the mesenchyme caused progressive loss of subepithelial fibroblasts and abbreviated gut length, revealing an unexpected requirement in this compartment. Surprisingly, constitutive Notch activity also induced rapid mesenchymal cell loss and impaired organogenesis, probably resulting from increased cell death and suggesting the need for a delicate balance in Notch signaling. Because digestive tract anomalies in mouse embryos with excess Notch activity phenocopy the absence of Hh signaling, we postulated that endodermal Hh restrains mesenchymal Notch pathway activity. Indeed, Hh-deficient embryos showed Notch overactivity in their defective gut mesenchyme and exposure to recombinant sonic hedgehog could override Notch-induced death of cultured fetal gut mesenchymal cells. These results reveal unexpected interactions between prominent signals in gastrointestinal development and provide a coherent explanation for Hh requirements in mesenchymal cell survival and organ growth.

PMID 21750033

2010

Salivary gland branching morphogenesis--recent progress and future opportunities

Int J Oral Sci. 2010 Sep;2(3):117-26.

Hsu JC, Yamada KM. Source Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892-4370, USA. Abstract Salivary glands provide saliva to maintain oral health, and a loss of salivary gland function substantially decreases quality-of-life. Understanding the biological mechanisms that generate salivary glands during embryonic development may identify novel ways to regenerate function or design artificial salivary glands. This review article summarizes current research on the process of branching morphogenesis of salivary glands, which creates gland structure during development. We highlight exciting new advances and opportunities in studies of cell-cell interactions, mechanical forces, growth factors, and gene expression patterns to improve our understanding of this important process.

PMID 21125789

Different thymosin Beta 4 immunoreactivity in foetal and adult gastrointestinal tract

PLoS One. 2010 Feb 9;5(2):e9111.

Nemolato S, Cabras T, Cau F, Fanari MU, Fanni D, Manconi B, Messana I, Castagnola M, Faa G.

Divisione di Anatomia Patologica, Dipartimento di Citomorfologia, University of Cagliari, Cagliari, Italy. Abstract BACKGROUND: Thymosin beta 4 (Tbeta(4)) is a member of beta-thymosins, a family of peptides that play essential roles in many cellular functions. A recent study from our group suggested a role for Tbeta(4) in the development of human salivary glands. The aim of this study was to analyze the expression of Tbeta(4) in the human gut during development, and in the adult.

METHODOLOGY/PRINCIPAL FINDINGS: Immunolocalization of Tbeta(4) was studied in autoptic samples of tongue, oesophagus, stomach, ileum, colon, liver and pancreas obtained from two human foetuses and two adults. Tbeta(4) appeared unevenly distributed, with marked differences between foetuses and adults. In the stomach, superficial epithelium was positive in foetuses and negative in adults. Ileal enterocytes were strongly positive in the adult and weakly positive in the foetuses. An increase in reactivity for Tbeta(4) was observed in superficial colon epithelium of adults as compared with the foetuses. Striking differences were found between foetal and adult liver: the former showed a very low reactivity for Tbeta(4) while in the adult we observed a strong reactivity in the vast majority of the hepatocytes. A peculiar pattern was found in the pancreas, with the strongest reactivity observed in foetal and adult islet cells.

SIGNIFICANCE: Our data show a strong expression of Tbeta(4) in the human gut and in endocrine pancreas during development. The observed differential expression of Tbeta(4) suggests specific roles of the peptide in the gut of foetuses and adults. The observed heterogeneity of Tbeta(4) expression in the foetal life, ranging from a very rare detection in liver cells up to a diffuse reactivity in endocrine pancreas, should be taken into account when the role of Tbeta(4) in the development of human embryo is assessed. Future studies are needed to shed light on the link between Tbeta(4) and organogenesis.

PMID 20161756

TGF-β2 Suppresses Macrophage Cytokine Production and Mucosal Inflammatory Responses in the Developing Intestine

Maheshwari A, Kelly DR, Nicola T, Ambalavanan N, Jain SK, Murphy-Ullrich J, Athar M, Shimamura M, Bhandari V, Aprahamian C, Dimmitt RA, Serra R, Ohls RK. Gastroenterology. 2010 Sep 24. [Epub ahead of print] PMID 20875417


"Premature neonates born before 32 weeks of gestation or with a birth weight <1500 grams are predisposed to necrotizing enterocolitis (NEC), an idiopathic, inflammatory bowel necrosis characterized by pneumatosis intestinalis (accumulation of gaseous products of bacterial fermentation within the bowel wall)"

"occurrence of NEC only after postnatal bacterial colonization and never in the sterile intrauterine microenvironment prior to birth"

"NEC is believed to occur when mucosal injury or altered permeability in the preterm intestine permits the translocation of luminal bacteria across the epithelial barrier, which, in turn, triggers a severe inflammatory response"

2009

Left-right asymmetry in gut development: what happens next?

Bioessays. 2009 Oct;31(10):1026-37. Burn SF, Hill RE. Source MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, Western General Hospital, Edinburgh, UK. Abstract 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.

PMID 19708022


The role of the visceral mesoderm in the development of the gastrointestinal tract

Gastroenterology. 2009 Jun;136(7):2074-91. Epub 2009 Mar 17.

McLin VA, Henning SJ, Jamrich M. Source Department of Pediatrics, Section of Gastroenterology, Hepatology and Nutrition, Baylor College of Medicine, Houston, Texas, USA. valerie.mclin@hcuge.ch Abstract The gastrointestinal (GI) tract forms from the endoderm (which gives rise to the epithelium) and the mesoderm (which develops into the smooth muscle layer, the mesenchyme, and numerous other cell types). Much of what is known of GI development has been learned from studies of the endoderm and its derivatives, because of the importance of epithelial biology in understanding and treating human diseases. Although the necessity of epithelial-mesenchymal cross talk for GI development is uncontested, the role of the mesoderm remains comparatively less well understood. The transformation of the visceral mesoderm during development is remarkable; it differentiates from a very thin layer of cells into a complex tissue comprising smooth muscle cells, myofibroblasts, neurons, immune cells, endothelial cells, lymphatics, and extracellular matrix molecules, all contributing to the form and function of the digestive system. Understanding the molecular processes that govern the development of these cell types and elucidating their respective contribution to GI patterning could offer insight into the mechanisms that regulate cell fate decisions in the intestine, which has the unique property of rapid cell renewal for the maintenance of epithelial integrity. In reviewing evidence from both mammalian and nonmammalian models, we reveal the important role of the visceral mesoderm in the ontogeny of the GI tract.

PMID 19303014

The serosal mesothelium is a major source of smooth muscle cells of the gut vasculature.

Wilm B, Ipenberg A, Hastie ND, Burch JB, Bader DM.

Most internal organs are situated in a coelomic cavity and are covered by a mesothelium. During heart development, epicardial cells (a mesothelium) move to and over the heart, undergo epithelial-mesenchymal transition (EMT), and subsequently differentiate into endothelial and vascular smooth muscle cells. This is thought to be a unique process in blood vessel formation. Still, structural and developmental similarities between the heart and gut led us to test the hypothesis that a conserved or related mechanism may regulate blood vessel development to the gut, which, similar to the heart, is housed in a coelomic cavity. By using a combination of molecular genetics, vital dye fate mapping, organ culture and immunohistochemistry, we demonstrate that the serosal mesothelium is the major source of vasculogenic cells in developing mouse gut. Our studies show that the gut is initially devoid of a mesothelium but that serosal mesothelial cells expressing the Wilm's tumor protein (Wt1) move to and over the gut. Subsequently, a subset of these cells undergoes EMT and migrates throughout the gut. Using Wt1-Cre genetic lineage marking of serosal cells and their progeny, we demonstrate that these cells differentiate to smooth muscle of all major blood vessels in the mesenteries and gut. Our data reveal a conserved mechanism in blood vessel formation to coelomic organs, and have major implications for our understanding of vertebrate organogenesis and vascular deficiencies of the gut.

PMID: 16284122


Pancreas cell fate

http://www.ncbi.nlm.nih.gov/pubmed/19750517

"Diabetes is characterized by decreased function of insulin-producing beta cells and insufficient insulin output resulting from an absolute (Type 1) or relative (Type 2) inadequate functional beta cell mass. Both forms of the disease would greatly benefit from treatment strategies that could enhance beta cell regeneration and/or function. Successful and reliable methods of generating beta cells or whole islets from progenitor cells in vivo or in vitro could lead to restoration of beta cell mass in individuals with Type 1 diabetes and enhanced beta cell compensation in Type 2 patients. A thorough understanding of the normal developmental processes that occur during pancreatic organogenesis, for example, transcription factors, cell signaling molecules, and cell-cell interactions that regulate endocrine differentiation from the embryonic pancreatic epithelium, is required in order to successfully reach these goals. This review summarizes our current understanding of pancreas development, with particular emphasis on factors intrinsic or extrinsic to the pancreatic epithelium that are involved in regulating the development and differentiation of the various pancreatic cell types. We also discuss the recent progress in generating insulin-producing cells from progenitor sources."


<pubmed>6502578</pubmed> <pubmed>18075226</pubmed>


Salivary gland branching morphogenesis: a quantitative systems analysis of the Eda/Edar/NFkappaB paradigm

BMC Dev Biol. 2009 Jun 6;9:32.

Melnick M, Phair RD, Lapidot SA, Jaskoll T. Source Laboratory for Developmental Genetics, USC, Los Angeles, CA, USA. mmelnick@usc.edu

Abstract

BACKGROUND: Ectodysplasin-A appears to be a critical component of branching morphogenesis. Mutations in mouse Eda or human EDA are associated with absent or hypoplastic sweat glands, sebaceous glands, lacrimal glands, salivary glands (SMGs), mammary glands and/or nipples, and mucous glands of the bronchial, esophageal and colonic mucosa. In this study, we utilized EdaTa (Tabby) mutant mice to investigate how a marked reduction in functional Eda propagates with time through a defined genetic subcircuit and to test the proposition that canonical NFkappaB signaling is sufficient to account for the differential expression of developmentally regulated genes in the context of Eda polymorphism.

RESULTS: The quantitative systems analyses do not support the stated hypothesis. For most NFkappaB-regulated genes, the observed time course of gene expression is nearly unchanged in Tabby (EdaTa) as compared to wildtype mice, as is NFkappaB itself. Importantly, a subset of genes is dramatically differentially expressed in Tabby (Edar, Fgf8, Shh, Egf, Tgfa, Egfr), strongly suggesting the existence of an alternative Eda-mediated transcriptional pathway pivotal for SMG ontogeny. Experimental and in silico investigations have identified C/EBPalpha as a promising candidate.

CONCLUSION: In Tabby SMGs, upregulation of the Egf/Tgfalpha/Egfr pathway appears to mitigate the potentially severe abnormal phenotype predicted by the downregulation of Fgf8 and Shh. Others have suggested that the buffering of the phenotypic outcome that is coincident with variant Eda signaling could be a common mechanism that permits viable and diverse phenotypes, normal and abnormal. Our results support this proposition. Further, if branching epithelia use variations of a canonical developmental program, our results are likely applicable to understanding the phenotypes of other branching organs affected by Eda (EDA) mutation.

PMID 19500387

1995

Morphological studies of the developing human esophageal epithelium

Microsc Res Tech. 1995 Jun 15;31(3):215-25. Ménard D. Source Département d'Anatomie et de Biologie Cellulaire, Faculté de Médecine, Université de Sherbrooke, Québec, Canada.

Abstract

This article focusses on the structural development of human esophageal ciliated epithelium. A combination of transmission electron microscopic (TEM), scanning electron microscopic (SEM), radioautographic, and light microscopic (LM) analyses were carried out using intact fetal tissues between 8 and 20 weeks of gestation as well as cultured esophageal explants. Up to the age of 10 weeks, the stratified esophageal epithelium consisted of two longitudinal primary folds. The surface cells were undifferentiated and contained large glycogen aggregates. Between 11 and 16 weeks, the primary folds (now up to four) had developed secondary folds. The thickness of the epithelium drastically increased (123%) in concomittance with a differentiation of surface columnar ciliated cells. These highly specialized surface cells exhibited junctional complexes and well-developed organelles with numerous microvilli interspersed among the cilia. Transverse sections revealed the internal structure of the cilia with a consistent pattern of nine doublet microtubules surrounding a central pair of single microtubules. Freeze-fracture studies illustrated the presence of a ciliary necklace composed of 6 ring-like rows of intramembranous particles. They also revealed the structure of ciliary cell tight junctions consisting of up to nine anastomosing strands (P-face) or complementary grooves (E-face). Ultrastructural studies (LM, TEM, SEM) of the esophageal squamous epithelium obtained after 15 days of culture showed that the newly formed epithelium was similar to adult human epithelium. Finally LM and SEM observations established that the esophagogastric junction was not yet well delineated, consisting of a transitional area composed of a mixture of esophageal ciliated cells and gastric columnar mucous cells.

PMID 7670160

Self Assessment Questions

  1. What is a pharyngeal arch and pouch? List the muscle, arch cartilage and nerves of each arch. List the derivatives of each pharyngeal pouch.
  2. Describe the main steps in the development of the tongue.
  3. What are the derivatives of the fore-, mid- and hind-gut?
  4. What is the buccopharyngeal membrane?
  5. How does the thyroid gland develop?
  6. Describe the normal development of the face and palate. List the major malformations of this region and their possible causes.
  7. How is the liver developed?
  8. What are the main processes involved in the elongation and rotation of the stomach and intestinal region?
  9. Describe the development of the pancreas.
  10. How does the myenteric plexus develop?
  11. List the basic principles in the development of the peritoneum.
  12. What are the functions of the liver and pancreas in the fetus? Does the gastro-intestinal tract function in the fetus?
  13. What are the consequences of malrotation of the gut?