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Cite this page: Hill, M.A. (2021, May 16) Embryology Endoderm. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Endoderm
Dnmt1 is required for proximal-distal patterning of the lung endoderm and for restraining alveolar type 2 cell fate
Dev Biol. 2019 Jun 23. pii: S0012-1606(19)30222-2. doi: 10.1016/j.ydbio.2019.06.019. [Epub ahead of print]
Liberti DC1, Zepp JA2, Bartoni CA2, Liberti KH3, Zhou S4, Lu M4, Morley MP2, Morrisey EE5.
Lung endoderm development occurs through a series of finely coordinated transcriptional processes that are regulated by epigenetic mechanisms. However, the role of DNA methylation in regulating lung endoderm development remains poorly understood. We demonstrate that DNA methyltransferase 1 (Dnmt1) is required for early branching morphogenesis of the lungs and for restraining epithelial fate specification. Loss of Dnmt1 leads to an early branching defect, a loss of epithelial polarity and proximal endodermal cell differentiation, and an expansion of the distal endoderm compartment. Dnmt1 deficiency also disrupts epithelial-mesenchymal crosstalk and leads to precocious distal endodermal cell differentiation with premature expression of alveolar type 2 cell restricted genes. These data reveal an important requirement for Dnmt1 mediated DNA methylation in early lung development to promote proper branching morphogenesis, maintain proximal endodermal cell fate, and suppress premature activation of the distal epithelial fate. Copyright © 2019. Published by Elsevier Inc.
PMID: 31242446 DOI: 10.1016/j.ydbio.2019.06.019
Enhancer, transcriptional, and cell fate plasticity precedes intestinal determination during endoderm development
Genes Dev. 2018 Nov 1;32(21-22):1430-1442. doi: 10.1101/gad.318832.118. Epub 2018 Oct 26.
Banerjee KK#1,2, Saxena M#1,2, Kumar N#3, Chen L3, Cavazza A1,2, Toke NH3, O'Neill NK1, Madha S1, Jadhav U1,2, Verzi MP3,4,5, Shivdasani RA1,2,6.
Abstract After acquiring competence for selected cell fates, embryonic primordia may remain plastic for variable periods before tissue identity is irrevocably determined (commitment). We investigated the chromatin basis for these developmental milestones in mouse endoderm, a tissue with recognizable rostro-caudal patterning and transcription factor (TF)-dependent interim plasticity. Foregut-specific enhancers are as accessible and active in early midgut as in foregut endoderm, and intestinal enhancers and identity are established only after ectopic cis-regulatory elements are decommissioned. Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. Thus, midgut endoderm is primed for heterologous cell fates, and TFs act on a background of shifting chromatin access to determine intestinal at the expense of foregut identity. Similar principles likely govern other fate commitments.
KEYWORDS: chromatin plasticity; developmental competence; developmental plasticity; fate determination; homeodomain transcription factors; lineage commitment; tissue specification PMID: 30366903 PMCID: PMC6217732 [Available on 2019-05-01] DOI: 10.1101/gad.318832.118
Distinct mechanisms for PDGF and FGF signaling in primitive endoderm development
Dev Biol. 2018 Jul 17. pii: S0012-1606(18)30415-9. doi: 10.1016/j.ydbio.2018.07.010. [Epub ahead of print]
Molotkov A1, Soriano P2. Author information
Abstract FGF signaling is known to play a critical role in the specification of primitive endoderm (PrE) and epiblast (Epi) from the inner cell mass (ICM) during mouse preimplantation development, but how FGFs synergize with other growth factor signaling pathways is unknown. Because PDGFRα signaling has also been implicated in the PrE, we investigated the coordinate functions of PDGFRα together with FGFR1 or FGFR2 in PrE development. PrE development was abrogated in Pdgfra; Fgfr1 compound mutants, or significantly reduced in Pdgfra; Fgfr2 or PdgfraPI3K; Fgfr2 compound mutants. We provide evidence that both Fgfr2 and Pdgfra play roles in PrE cell survival while Fgfr1 controls PrE cell specification. Our results suggest a model where FGFR1-engaged ERK1/2 signaling governs PrE specification while PDGFRα- and by analogy possibly FGFR2- engaged PI3K signaling regulates PrE survival and positioning in the embryo. Together, these studies indicate how multiple growth factors and signaling pathways can cooperate in preimplantation development. KEYWORDS: Cell specification; ERK1/2; PI3K; Preimplantation; Survival
Nucleoporin 107, 62 and 153 mediate Kcnq1ot1 imprinted domain regulation in extraembryonic endoderm stem cells
Nat Commun. 2018 Jul 18;9(1):2795. doi: 10.1038/s41467-018-05208-2.
Sachani SS1,2,3,4, Landschoot LS1,2, Zhang L1,2, White CR1,2, MacDonald WA3,4, Golding MC5, Mann MRW6,7.
Genomic imprinting is a phenomenon that restricts transcription to predominantly one parental allele. How this transcriptional duality is regulated is poorly understood. Here we perform an RNA interference screen for epigenetic factors involved in paternal allelic silencing at the Kcnq1ot1 imprinted domain in mouse extraembryonic endoderm stem cells. Multiple factors are identified, including nucleoporin 107 (NUP107). To determine NUP107's role and specificity in Kcnq1ot1 imprinted domain regulation, we deplete Nup107, as well as Nup62, Nup98/96 and Nup153. Nup107, Nup62 and Nup153, but not Nup98/96 depletion, reduce Kcnq1ot1 noncoding RNA volume, displace the Kcnq1ot1 domain from the nuclear periphery, reactivate a subset of normally silent paternal alleles in the domain, alter histone modifications with concomitant changes in KMT2A, EZH2 and EHMT2 occupancy, as well as reduce cohesin interactions at the Kcnq1ot1 imprinting control region. Our results establish an important role for specific nucleoporins in mediating Kcnq1ot1 imprinted domain regulation.
Different murine-derived feeder cells alter the definitive endoderm differentiation of human induced pluripotent stem cells
PLoS One. 2018 Jul 26;13(7):e0201239. doi: 10.1371/journal.pone.0201239. eCollection 2018.
Shoji M1, Minato H1, Ogaki S2, Seki M3, Suzuki Y3, Kume S2, Kuzuhara T1.
Abstract The crosstalk between cells is important for differentiation of cells. Murine-derived feeder cells, SNL76/7 feeder cells (SNLs) or mouse primary embryonic fibroblast feeder cells (MEFs) are widely used for culturing undifferentiated human induced pluripotent stem cells (hiPSCs). It is still unclear whether different culture conditions affect the induction efficiency of definitive endoderm (DE) differentiation from hiPSCs. Here we show that the efficiency of DE differentiation from hiPSCs cultured on MEFs was higher than that of hiPSCs cultured on SNLs. The qPCR, immunofluorescent and flow cytometry analyses revealed that the expression levels of mRNA and/or proteins of the DE marker genes, SOX17, FOXA2 and CXCR4, in DE cells differentiated from hiPSCs cultured on MEFs were significantly higher than those cultured on SNLs. Comprehensive RNA sequencing and molecular network analyses showed the alteration of the gene expression and the signal transduction of hiPSCs cultured on SNLs and MEFs. Interestingly, the expression of non-coding hXIST exon 4 was up-regulated in hiPSCs cultured on MEFs, in comparison to that in hiPSCs cultured on SNLs. By qPCR analysis, the mRNA expression of undifferentiated stem cell markers KLF4, KLF5, OCT3/4, SOX2, NANOG, UTF1, and GRB7 were lower, while that of hXIST exon 4, LEFTY1, and LEFTY2 was higher in hiPSCs cultured on MEFs than in those cultured on SNLs. Taken together, our finding indicated that differences in murine-feeder cells used for maintenance of the undifferentiated state alter the expression of pluripotency-related genes in hiPSCs by the signaling pathways and affect DE differentiation from hiPSCs, suggesting that the feeder cells can potentiate hiPSCs for DE differentiation.
|Adult Cells - derived from Endoderm|
|Adult Cells Embryonic Origin: Endoderm | Mesoderm | Ectoderm|
|Exocrine secretory epithelial cells|
|Endocrine System Development - Hormone-secreting cells|
Cas9-mediated excision of Nematostella brachyury disrupts endoderm development, pharynx formation and oral-aboral patterning
Development. 2017 Aug 15;144(16):2951-2960. doi: 10.1242/dev.145839. Epub 2017 Jul 13.
Servetnick MD1, Steinworth B2, Babonis LS2, Simmons D2, Salinas-Saavedra M2, Martindale MQ2.
Abstract The mesoderm is a key novelty in animal evolution, although we understand little of how the mesoderm arose. brachyury, the founding member of the T-box gene family, is a key gene in chordate mesoderm development. However, the brachyury gene was present in the common ancestor of fungi and animals long before mesoderm appeared. To explore ancestral roles of brachyury prior to the evolution of definitive mesoderm, we excised the gene using CRISPR/Cas9 in the diploblastic cnidarian Nematostella vectensisNvbrachyury is normally expressed in precursors of the pharynx, which separates endoderm from ectoderm. In knockout embryos, the pharynx does not form, embryos fail to elongate, and endoderm organization, ectodermal cell polarity and patterning along the oral-aboral axis are disrupted. Expression of many genes both inside and outside the Nvbrachyury expression domain is affected, including downregulation of Wnt genes at the oral pole. Our results point to an ancient role for brachyury in morphogenesis, cell polarity and the patterning of both ectodermal and endodermal derivatives along the primary body axis. KEYWORDS: Brachyury; Cnidarian; Endoderm; Mesoderm; Nematostella; Pharynx PMID: 28705897 PMCID: PMC5592810 DOI: 10.1242/dev.145839
Endoderm Derived Cells
Exocrine secretory epithelial cells
- Salivary gland mucous cell (polysaccharide-rich secretion)
- Salivary gland number 1 (glycoprotein enzyme-rich secretion)
- Von Ebner's gland cell in tongue (washes taste buds)
- Mammary gland cell (milk secretion)
- Lacrimal gland cell (tear secretion)
- Ceruminous glands|Ceruminous gland cell in ear (earwax secretion)
- Eccrine sweat glands|Eccrine sweat gland dark cell (glycoprotein secretion)
- Eccrine sweat glands|Eccrine sweat gland clear cell (small molecule secretion)
- Apocrine sweat glands|Apocrine sweat gland cell (odoriferous secretion, sex-hormone sensitive)
- Gland of Moll cell in eyelid (specialized sweat gland)
- Sebaceous gland cell (lipid-rich sebum secretion)
- Bowman's gland cell in human nose|nose (washes olfactory epithelium)
- Brunner's gland cell in duodenum (enzymes and alkaline mucus)
- Seminal vesicle cell (secretes seminal fluid components, including fructose for swimming Spermatozoon|sperm)
- Prostate gland cell (secretes seminal fluid components)
- Bulbourethral gland cell (mucus secretion)
- Bartholin's gland cell (vaginal lubricant secretion)
- Urethral gland|Gland of Littre cell (mucus secretion)
- Uterus endometrium cell (carbohydrate secretion)
- Insolated goblet cell of respiratory tract|respiratory and Gastrointestinal tract|digestive tracts (mucus secretion)
- Stomach lining mucous cell (mucus secretion)
- Gastric chief cell|Gastric gland zymogenic cell (pepsinogen secretion)
- Parietal cell - Gastric gland oxyntic cell (hydrochloric acid secretion)
- Pancreatic acinar cell (bicarbonate and digestive enzyme secretion
- Paneth cell of small intestine (lysozyme secretion)
- Type II pneumocyte of human lung (surfactant secretion)
- Club cell of lung
- Anterior pituitary cells
- Intermediate pituitary cell, secreting melanocyte-stimulating hormone
- Magnocellular neurosecretory cells
- nonsecreting oxytocin
- secreting vasopressin
- Gut and respiratory tract cells
- secreting serotonin
- secreting endorphin
- secreting somatostatin
- secreting gastrin
- secreting secretin
- nonsecreting cholecystokinin
- secreting insulin
- secreting glucagon
- nonsecreting bombesin
- Thyroid gland cells
- Thyroid epithelial cell
- Parafollicular cell
- Parathyroid gland cells
- Parathyroid chief cell
- Oxyphil cell (parathyroid)|Oxyphil cell
- Adrenal gland cells
- Chromaffin cells
- secreting steroid hormones (mineralocorticoids and gluco corticoids)
- Leydig cell of testes secreting testosterone
- Theca interna cell of ovarian follicle secreting estrogen
- Corpus luteum cell of ruptured ovarian follicle secreting progesterone
- Granulosa lutein cells
- Theca lutein cells
- Juxtaglomerular cell (renin secretion)
- Macula densa cell of kidney
- Peripolar cell of kidney
- Mesangial cell of kidney
- Pancreatic islets (islets of Langerhans)
- Alpha cells (secreting glucagon)
- Beta cells (secreting insulin and amylin)
- Delta cells (secreting somatostatin)
- PP cells (gamma cells) (secreting pancreatic polypeptide)
- Epsilon cells (secreting ghrelin)
Late stage definitive endodermal differentiation can be defined by Daf1 expression
BMC Dev Biol. 2016 May 31;16(1):19. doi: 10.1186/s12861-016-0120-2.
Ogaki S1,2,3, Omori H2, Morooka M2, Shiraki N1, Ishida S3, Kume S4,5.
BACKGROUND: Definitive endoderm (DE) gives rise to the respiratory apparatus and digestive tract. Sox17 and Cxcr4 are useful markers of the DE. Previously, we identified a novel DE marker, Decay accelerating factor 1(Daf1/CD55), by identifying DE specific genes from the expression profile of DE derived from mouse embryonic stem cells (ESCs) by microarray analysis, and in situ hybridization of early embryos. Daf1 is expressed in a subpopulation of E-cadherin + Cxcr4+ DE cells. The characteristics of the Daf1-expressing cells during DE differentiation has not been examined. RESULTS: In this report, we utilized the ESC differentiation system to examine the characteristics of Daf1-expressing DE cells. We found that Daf1 expression could discriminate late DE from early DE. Early DE cells are Daf1-negative (DE-) and late DE cells are Daf1-positive (DE+). We also found that Daf1+ late DE cells show low proliferative and low cell matrix adhesive characteristics. Furthermore, the purified SOX17(low) early DE cells gave rise to Daf1+ Sox17(high) late DE cells. CONCLUSION: Daf1-expressing late definitive endoderm proliferates slowly and show low adhesive capacity. KEYWORDS: Adhesion; Daf1; Definitive endoderm; In vitro differentiation; Pluripotent stem cell; Proliferation
Role of the gut endoderm in relaying left-right patterning in mice
PLoS Biol. 2012 Mar;10(3):e1001276. Epub 2012 Mar 6. Viotti M, Niu L, Shi SH, Hadjantonakis AK. Source Developmental Biology Program, Sloan-Kettering Institute, New York, New York, United States of America.
Establishment of left-right (LR) asymmetry occurs after gastrulation commences and utilizes a conserved cascade of events. In the mouse, LR symmetry is broken at a midline structure, the node, and involves signal relay to the lateral plate, where it results in asymmetric organ morphogenesis. How information transmits from the node to the distantly situated lateral plate remains unclear. Noting that embryos lacking Sox17 exhibit defects in both gut endoderm formation and LR patterning, we investigated a potential connection between these two processes. We observed an endoderm-specific absence of the critical gap junction component, Connexin43 (Cx43), in Sox17 mutants. Iontophoretic dye injection experiments revealed planar gap junction coupling across the gut endoderm in wild-type but not Sox17 mutant embryos. They also revealed uncoupling of left and right sides of the gut endoderm in an isolated domain of gap junction intercellular communication at the midline, which in principle could function as a barrier to communication between the left and right sides of the embryo. The role for gap junction communication in LR patterning was confirmed by pharmacological inhibition, which molecularly recapitulated the mutant phenotype. Collectively, our data demonstrate that Cx43-mediated communication across gap junctions within the gut endoderm serves as a mechanism for information relay between node and lateral plate in a process that is critical for the establishment of LR asymmetry in mice.
Formation of the murine endoderm lessons from the mouse, frog, fish, and chick
Prog Mol Biol Transl Sci. 2010;96:1-34.
Abstract The mammalian definitive endoderm arises as a simple epithelial sheet. This sheet of cells will eventually produce the innermost tube that comprises the entire digestive tract from the esophagus to the colon as well as the epithelial component of the digestive and respiratory organs including the thymus, thyroid, lung, liver, gallbladder, and pancreas. Thus a wide array of tissue types are derived from the early endodermal sheet, and understanding the morphological and molecular mechanisms used to produce this tissue is integral to understanding the development of all these organs. The goal of this chapter is to summarize what is known about the morphological and molecular mechanisms used to produce this embryonic germ layer. Although this chapter mainly focuses on the mechanisms used to generate the murine endoderm, supportive or suggestive data from other species, including chick, frog (Xenopus laevis), and the Zebrafish (Danio rerio) are also examined.
Copyright © 2010 Elsevier Inc. All rights reserved. PMID: 21075338
Vertebrate Endoderm Development and Organ Formation http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2861293/?tool=pubmed
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