Reciprocal endoderm-mesoderm interactions mediated by<i>fgf24</i>and<i>fgf10</i>govern pancreas development

Manfroid, Isabelle; Delporte, François M; Baudhuin, Ariane; Motté, Patrick; Neumann, Carl J.; Voz, Marianne L.; Martial, Joseph; Peers, Bernard

doi:10.1242/dev.007823

Cited by 59 publications

(64 citation statements)

References 51 publications

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“…Although Meis3 seems to have a more restricted expression pattern than the other two Meis genes in mouse, Xenopus, and zebrafish (Waskiewicz et al, 2001;Ng et al, 2009), it has been implicated in several developmental processes in these species (Dibner et al, 2001(Dibner et al, , 2004Aamar and Frank, 2004;diIorio et al, 2007;Manfroid et al, 2007;Elkouby et al, 2010;Gutkovich et al, 2010). However, these roles could represent evolutionary novelties or cooptions in these lineages or, alternatively, could have been taken over by the other Meis genes in birds.…”

Section: Discussionmentioning

confidence: 99%

Distinct and redundant expression and transcriptional diversity of MEIS gene paralogs during chicken development

Sánchez-Guardado

Irimia

Sánchez-Arrones

et al. 2011

Developmental Dynamics

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Members of the Meis family of TALE homeobox transcription factors are involved in many processes of vertebrate development and morphogenesis, showing extremely complex transcriptional and spatiotemporal expression patterns. In this work, we performed a comprehensive study of chicken Meis genes using multiple approaches. First, we assessed whether the chicken genome contains a Meis3 ortholog or harbors only two Meis genes; we gathered several lines of evidence pointing to a specific loss of the Meis3 ortholog in an early ancestor of birds. Next, we studied the transcriptional diversity generated from chicken Meis genes through alternative splicing during development. Finally, we performed a detailed analysis of chick Meis1/ 2 expression patterns during early embryogenesis and organogenesis. We show that the expression of both Meis genes begins at the gastrulation stage in the three embryonic layers, presenting highly dynamic patterns with overlapping as well as distinct expression domains throughout development. Developmental Dynamics 240:1475-1492, 2011. V C 2011 Wiley-Liss, Inc.Key words: TALE family; alternative splicing; ectoderm; mesoderm; endoderm; central nervous system; sensory organs; visceral development; gut Accepted 17 January 2011 Developmental DynamicsABBREVIATIONS A atrium aip anterior intestinal portal as alternative splicing av allantoic vesicle ba branchial arches bd bile duct C conotruncus cl cloaca cnp caudal neural plate co coelom cp cardiac primordium D diencephalon da dorsal aorta dh dorsal horn dm dermomyotome dp dorsal pancreas du duodenum ect ectoderm ep ephiphysis end endoderm Eo-PmC extraocular pre-muscle cluster FB forebrain fg foregut fp floor plate Hn Hensen node HB hindbrain Hyp hypothalamus inf infundibulum isth isthmus l lens ltl larynx-trachea-lug bud lpm lateral plate mesoderm lp lens placode lv liver lb lung bud MB midbrain Mes mesencephalon mes mesoderm mg mid-gut mn mesonephric system mp mandibular process MRB mesencephalic-rhombencephalic boundary nep nephrotome nf neural fold np neural plate nr neural retina nt notochord oc otic cup oe oesophagus of optic furrow omv omphalomensenteric vena os optic stalk ot otocyst ov optic vesicle p prosomere p1 prosomere 1 p2 prosomere 2 p3 prosomere 3 pc pericardial cavity pe pigmented epithelium pf primitive fold pg primitive groove ph pharynx pm precardiac mesoderm POA preoptic area pp prechordal plate ps primitive streak psm primitive streak mesoderm PT pretectum Rh rhombencephalon rh rhombomere RhA1 rhombomere A1 rnp rostral neural plate Rp Rathke's pouch rp roof plate SC spinal cord scl sclerotome sm somatic mesoderm smp somatopleure som somite SP secondary prosencephalon sp segmental plate spm splanchnic mesoderm spp splanchnopleure st stomach sub.p subcephalic pocket sv sinus venosus tb tail bud td thyro-glossal duct Tel telencephalon TH thalamus Tv telencephalic vesicle V.n trigeminal ganglion V ventricle WGS whole genome shotgun zli zona limitans intrathalamica

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Section: Discussionmentioning

confidence: 99%

Distinct and redundant expression and transcriptional diversity of MEIS gene paralogs during chicken development

Sánchez-Guardado

Irimia

Sánchez-Arrones

et al. 2011

Developmental Dynamics

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“…fgf10a knockdown greatly enhances ectopic hepatocyte formation induced by Wnt8a overexpression We next sought to identify the Fgf ligand(s) that negatively regulate hepatic competence. We first tested fgf10a because it is expressed in the mesenchyme surrounding the endoderm that gives rise to the pancreas and intestinal bulb (Dong et al, 2007;Manfroid et al, 2007), and fgf10a mutants occasionally exhibit a few ectopic hepatocytes in the proximal pancreas (Dong et al, 2007). We examined the expression pattern of fgf10a in greater detail.…”

Section: Research Articlementioning

confidence: 99%

Restriction of hepatic competence by Fgf signaling

et al. 2011

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SUMMARYHepatic competence, or the ability to respond to hepatic-inducing signals, is regulated by a number of transcription factors broadly expressed in the endoderm. However, extrinsic signals might also regulate hepatic competence, as suggested by tissue explant studies. Here, we present genetic evidence that Fgf signaling regulates hepatic competence in zebrafish. We first show that the endoderm posterior to the liver-forming region retains hepatic competence: using transgenic lines that overexpress hepatic inducing signals following heat-shock, we found that at late somitogenesis stages Wnt8a, but not Bmp2b, overexpression could induce liver gene expression in pancreatic and intestinal bulb cells. These manipulations resulted in the appearance of ectopic hepatocytes in the intestinal bulb. Second, by overexpressing Wnt8a at various stages, we found that as embryos develop, the extent of the endodermal region retaining hepatic competence is gradually reduced. Most significantly, we found, using gainand loss-of-function approaches, that Fgf10a signaling regulates this gradual reduction of the hepatic-competent domain. These data provide in vivo evidence that endodermal cells outside the liver-forming region retain hepatic competence and show that an extrinsic signal, Fgf10a, negatively regulates hepatic competence.

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“…We noticed an upregulation of dhrs3 expression in some ring1b embryos at 15 ss (Fig. 4H), which could reflect increased RA signaling or increased response to RA signaling.To address a possible deregulation of RA signaling further, we stained for dhrs3, hoxb5b and meis3, another RA-target gene expressed in the pectoral fin field, at 20 ss and 32 hpf (Gongal and Waskiewicz, 2008;Kudoh et al, 2002;Manfroid et al, 2007). The expression of hoxb5, meis3 and dhrs3 was indistinguishable from wild-type embryos at 20 ss (Fig.…”

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confidence: 98%

The Polycomb group protein Ring1b is essential for pectoral fin development

et al. 2012

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SUMMARYPolycomb group (PcG) proteins are transcriptional repressors that mediate epigenetic gene silencing by chromatin modification. PcG-mediated gene repression is implicated in development, cell differentiation, stem-cell fate maintenance and cancer. However, analysis of the roles of PcG proteins in orchestrating vertebrate developmental programs in vivo has been hampered by the early embryonic lethality of several PcG gene knockouts in mice. Here, we demonstrate that zebrafish Ring1b, the E3 ligase in Polycomb Repressive Complex 1 (PRC1), is essential for pectoral fin development. We show that differentiation of lateral plate mesoderm (LPM) cells into presumptive pectoral fin precursors is initiated normally in ring1b mutants, but fin bud outgrowth is impaired. Fgf signaling, which is essential for migration, proliferation and cell-fate maintenance during fin development, is not sufficiently activated in ring1b mutants. Exogenous application of FGF4, as well as enhanced stimulation of Fgf signaling by overactivated Wnt signaling in apc mutants, partially restores the fin developmental program. These results reveal that, in the absence of functional Ring1b, fin bud cells fail to execute the pectoral fin developmental program. Together, our results demonstrate that PcG-mediated gene regulation is essential for sustained Fgf signaling in vertebrate limb development. KEY WORDS: Ring1b, Zebrafish, FGF signaling, Fin, PolycombThe Polycomb group protein Ring1b is essential for pectoral fin development Yme U. van der Velden, Liqin Wang, Maarten van Lohuizen and Anna-Pavlina G. Haramis* , ‡ , 2000;Furthauer et al., 2001). From 15 ss onwards, heart precursors migrate medially to form the heart tube at the 20 ss (19 hpf). The more posteriorly located fin precursors condense into a compact fin field. Notably, tbx5 is the earliest known marker of prospective pectoral fin mesenchyme and is essential for the migration of these precursors (Ahn et al., 2002). DEVELOPMENT 2211 RESEARCH ARTICLERing1b controls fin development and InghamFin-mesenchyme compaction proceeds through Tbx5-mediated activation of fibroblast growth factor 24 (Fgf24), a teleost-specific Fgf and the first family member to be expressed in the pectoral fin mesenchyme (Fischer et al., 2003). Fgf24 signaling is required for both maintaining tbx5 expression and inducing fgf10 expression in the LPM cells, possibly through binding to Fgf receptor 2 (Fgfr2) (Fischer et al., 2003;Harvey and Logan, 2006). In turn, Fgf10 maintains fgf24 expression and contributes to the induction of the apical ectodermal ridge (AER), a signaling center that promotes outgrowth of the pectoral fin, starting at 28 hpf (Norton et al., 2005). Fgf10 signaling is then uniquely required for maintenance of AER function. Notably, fgf24 expression in the fin mesenchyme is downregulated at around 32 hpf, and ectodermal expression commences (Fischer et al., 2003). AER-derived Fgfs signal back to the pectoral fin mesenchyme to maintain fgf10 expression, thereby creating a positive-feedback loop i...

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Reciprocal endoderm-mesoderm interactions mediated byfgf24andfgf10govern pancreas development

Cited by 59 publications

References 51 publications

Distinct and redundant expression and transcriptional diversity of MEIS gene paralogs during chicken development

Distinct and redundant expression and transcriptional diversity of MEIS gene paralogs during chicken development

Restriction of hepatic competence by Fgf signaling

The Polycomb group protein Ring1b is essential for pectoral fin development

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