Region‐specific expression of murine <i>Hox </i>genes implies the <i>Hox</i> code‐mediated patterning of the digestive tract

Sekimoto, Tomohisa; Yoshinobu, Kumiko; Yoshida, Michio; Kuratani, Shigeru; Fujimoto, Shin; Araki, Masatake; Tajima, Naoya; Araki, Kimi; Yamamura, Ken‐ichi

doi:10.1046/j.1365-2443.1998.00167.x

Cited by 50 publications

(44 citation statements)

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“…In between, the gene hex regulates liver and thyroid development (Martinez Barbera et al, 2000;Keng et al, 2000). Genes belonging to the 4 Hox-clusters become extensively divided in endodermal compartments (Sekimoto et al, 1998;Kawazoe et al, 2002;Beck, 2002). However, these genes are not specific to the endoderm and are equally important in patterning the other germ layers, where they have been studied in more detail (Hunt and Krumlauf, 1991;Tam and Trainor, 1994;Trainor and Krumlauf, 2001).…”

Section: A "Core Endodermal Program"-and Variationsmentioning

confidence: 99%

Gene regulatory factors in pancreatic development

Jensen

2003

Developmental Dynamics

348

289

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The intensity of research on pancreatic development has increased markedly in the past 5 years, primarily for two reasons: we now know that the insulin-producing ␤-cells normally arise from an endodermally derived, pancreasspecified precursor cell, and successful transplants of islet cells have been performed, relieving patients with type I diabetes of symptoms for extended periods after transplantation. Combining in vitro ␤-cell formation from a pancreatic biopsy of a diabetic patient or from other stem-cell sources followed by endocrine cell transplantation may be the most beneficial route for a future diabetes therapy. However, to achieve this, a thorough understanding of the genetic components regulating the development of ␤-cells is required. The following review discusses our current understanding of the transcription factor networks necessary for pancreatic development and how several genetic interactions coming into play at the earliest stages of endodermal development gradually help to build the pancreatic organ.

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Section: A "Core Endodermal Program"-and Variationsmentioning

confidence: 99%

Gene regulatory factors in pancreatic development

Jensen

2003

Developmental Dynamics

348

289

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“…The RNA probes used to detect HoxD expression were the following: Hoxd1 (Zakany et al, 2001), Hoxd3 (Condie and Capecchi, 1993), Hoxd4 (Featherstone et al, 1988), Hoxd8 (Izpisua-Belmonte et al, 1990), Hoxd9 (Zappavigna et al, 1991), Hoxd10 and Hoxd11 (Gerard et al, 1996), Hoxd12 , Hoxd13 . The remaining RNA probes were Hoxa6 (Sekimoto et al, 1998), Hoxa10 (Favier et al, 1996), Fgf10 (Bellusci et al, 1997) and Pitx1 (Logan et al, 1998). For the complementation assay, newborns were recovered, their full GI was dissected, documented and genotyped.…”

Section: Gastrointestinal Tract Dissection and Whole-mount In Situ Hymentioning

confidence: 99%

“…While systematic analyses of expression patterns in mice have revealed a coordinated expression strategy (Sekimoto et al, 1998;Pitera et al, 1999;Kawazoe et al, 2002), more recent studies employing various methodologies of gene expression profiling have also supported the involvement of many Hox genes, including those in the HoxD cluster, in regionalization (Bates et al, 2002;Choi et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…A large number of Hox genes are coexpressed in posterior midgut, in a region that coincides with the future budding of the caecum Kawazoe et al, 2002;Levin et al, 1997;Pitera et al, 1999;Roberts et al, 1995;Sekimoto et al, 1998). By contrast, the expression of the most 'posterior' Hox genes, such as Hoxd12 and Hoxd13 is excluded from this precise region Kmita et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Hox gene function in vertebrate gut morphogenesis: the case of the caecum

2007

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The digestive tract is made of different subdivisions with various functions. During embryonic development, the developing intestine expresses combinations of Hox genes along its anterior to posterior axis, suggesting a role for these genes in this regionalization process. In particular, the transition from small to large intestine is labelled by the transcription of all Hoxd genes except Hoxd12 and Hoxd13, the latter two genes being transcribed only near the anus. Here, we describe two lines of mice that express Hoxd12 ectopically within this morphological transition. As a consequence, budding of the caecum is impeded, leading to complete agenesis in homozygous individuals. This effect is concurrent with a dramatic reduction of both Fgf10 and Pitx1 expression. Furthermore, the interactions between 'anterior' Hox genes and ectopic Hoxd12 suggest a model whereby anterior and posterior Hox products compete in controlling Fgf10 signalling, which is required for the growth of this organ in mice. These results illuminate components of the genetic cascade necessary for the emergence of this gut segment, crucial for many vertebrates.

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“…Formation of these sphincters is controlled by regionally specific expression of transcription factors (HOX genes) and morphogens (Smith and Tabin, 1999;Zakany and Duboule, 1999). HOX genes, which are collinearly expressed along the length of the GI tract, can be spatially and temporally correlated with morphological specialization, suggesting that they may pattern the GI tract along the rostrocaudal axis (Kawazoe et al, 2002;Pitera et al, 1999;Roberts, 2000;Sekimoto et al, 1998;Yokouchi et al, 1995). In addition to regional specification by these early patterning genes, epithelial-mesenchymal interactions function to further guide gut morphogenesis.…”

Section: Research Articlementioning

confidence: 99%

Reciprocal epithelial-mesenchymal FGF signaling is required for cecal development

et al. 2006

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Fibroblast growth factor (FGF) signaling mediates reciprocal mesenchymal-epithelial cell interactions in the developing mouse lung and limb. In the gastrointestinal (GI) tract, FGF10 is expressed in the cecal mesenchyme and signals to an epithelial splice form of FGF receptor (FGFR) 2 to regulate epithelial budding. Here, we identify FGF9 as a reciprocal epithelial-mesenchymal signal required for cecal morphogenesis. Fgf9 null (Fgf9 -/-) mouse embryos have agenesis of the embryonic cecum, lacking both mesenchymal expansion and an epithelial bud. In the cecal region of Fgf9 -/-embryos, mesenchymal expression of Fgf10 and Bmp4 is notably absent, whereas the expression of epithelial markers, such as sonic hedgehog, is not affected. Using epithelial and whole explant cultures, we show that FGF9 signals to mesenchymal FGFRs and that FGF10 signals to epithelial FGFRs. Taken together, these data show that an epithelial FGF9 signal is necessary for the expansion of cecal mesenchyme and the expression of mesenchymal genes that are required for epithelial budding. Thus, these data add to our understanding of FGF-mediated reciprocal epithelialmesenchymal signaling.

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Region‐specific expression of murine Hox genes implies the Hox code‐mediated patterning of the digestive tract

Cited by 50 publications

References 50 publications

Gene regulatory factors in pancreatic development

Gene regulatory factors in pancreatic development

Hox gene function in vertebrate gut morphogenesis: the case of the caecum

Reciprocal epithelial-mesenchymal FGF signaling is required for cecal development

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