Role of the FGF and MEK signaling pathway in the ascidian embryo

Kim, Gil Jung; Nishida, Hiroki

doi:10.1046/j.1440-169x.2001.00594.x

Cited by 89 publications

(141 citation statements)

References 62 publications

(80 reference statements)

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“…FGF signaling is mediated in vertebrate embryos by the Ras/MEK/MAPK cascade. In ascidians, these intermediates have been shown to play a conserved role during formation of the secondary notochord cells, as well as in the specification of the neural tissue (Kim and Nishida, 2001;Hudson et al, 2003).…”

Section: Larval Tissues Notochordmentioning

confidence: 99%

Ciona intestinalis: Chordate development made simple

2005

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Thanks to their transparent and rapidly developing mosaic embryos, ascidians (or sea squirts) have been a model system for embryological studies for over a century. Recently, ascidians have entered the postgenomic era, with the sequencing of the Ciona intestinalis genome and the accumulation of molecular resources that rival those available for fruit flies and mice. One strength of ascidians as a model system is their close similarity to vertebrates. Literature reporting molecular homologies between vertebrate and ascidian tissues has flourished over the past 15 years, since the first ascidian genes were cloned. However, it should not be forgotten that ascidians diverged from the lineage leading to vertebrates over 500 million years ago. Here, we review the main similarities and differences so far identified, at the molecular level, between ascidian and vertebrate tissues and discuss the evolution of the compact ascidian genome.

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Section: Larval Tissues Notochordmentioning

confidence: 99%

Ciona intestinalis: Chordate development made simple

2005

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“…In ascidians, however, blockade of FGF signaling by treatment with a MEK inhibitor or an FGF receptor inhibitor, or by injection of FGF MO does not alter the cleavage pattern up to the 64-cell stage (Kim and Nishida, 2001;Kumano et al, 2006) (present study). Thus, it is likely that FGF signaling is not involved in orientation of the mitotic spindles and cleavage planes in ascidian embryos.…”

Section: Research Articlementioning

confidence: 49%

“…1C) (reviewed by Nishida, 2005). When the inductive influence is inhibited by isolation of the blastomeres or using inhibitors of FGF signaling, both daughters of the mesenchyme/muscle and notochord/nerve cord precursors assume the default muscle and nerve cord fates, respectively (Kim et al, 2000;Minokawa et al, 2001;Kim and Nishida, 2001). In contrast, when the mother precursors are isolated and treated with FGF protein over their entire surface, both the daughter cells adopt the induced mesenchyme and notochord fates (Nakatani et al, 1996;Kim et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Consistently, the nerve cord/notochord precursors lose their competence to respond to the treatment of FGF protein at the division to the 64-cell stage (Nakatani et al, 1996). In addition, the sensitive period to the FGF receptor and MEK inhibitors ends at the sixth cleavage, suggesting that notochord induction completes during the 32-cell stage (Kim and Nishida, 2001). As to the division of the muscle/mesenchyme precursors, the precursors acquire the ability of autonomous mesenchyme formation in isolation sometime in the last half of the cell cycle at the 32-cell stage, indicating that mesenchyme induction also completes during that stage (Kim and Nishida, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Cell fate polarization in ascidian mesenchyme/muscle precursors by directed FGF signaling and role for an additional ectodermal FGF antagonizing signal in notochord/nerve cord precursors

2007

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Asymmetric cell division plays a fundamental role in generating various types of embryonic cell. In ascidian embryos, asymmetric cell divisions occur in the vegetal hemisphere in a manner similar to those found in Caenorhabditis elegans. Early divisions in embryos of both species involve inductive events on a single mother cell that result in production of daughters with different cell fates. Here we show in the ascidian Halocynthia roretzi that polarity of muscle/mesenchyme mother precursors is determined solely by the direction from which the FGF9/16/20 signal is presented, a role similar to that of Wnt signaling in the EMS and T cell divisions in C. elegans. However, polarity of nerve cord/notochord mother precursors is determined by possible antagonistic action between the FGF signal and a signal from anterior ectoderm, providing a new mechanism underlying asymmetric cell division. The ectoderm signal suppresses MAPK activation and expression of Hr-FoxA, which encodes an intrinsic competence factor for notochord induction, in the nerve cord lineage.

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“…Activation of the FGFR by ligand binding stimulates many downstream signaling cascades including the MAPK pathway; 33 MAPK plays a role in the early signaling events of FGF-mediated mesoderm induction in Xenopus. 34 The phosphorylation of Cdc25C by pp90 Rsk may contribute to the growth arrest that occurs during embryonic patterning.…”

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confidence: 99%

Phosphorylation of Cdc25C by pp90Rsk Contributes to a G2 Cell Cycle Arrest in Xenopus Cycling Egg Extracts

Chun

Chau²,

Maingat³

et al. 2004

Cell Cycle

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In unfertilized Xenopus eggs, the p42 mitogen activated protein kinase (p42MAPK) pathway is known to maintain cell cycle arrest at metaphase of meiosis II. However, constitutive activation of p42MAPK in post-meiotic, cycling Xenopus egg extracts can lead to either a G 2 or M-phase arrest of the cell cycle, depending on the timing of p42MAPK activation. Here, we examined the molecular mechanism by which activation of the p42MAPK pathway during interphase leads to cell cycle arrest in G 2 . When either a recombinant wild type Cdc25C(WT) or a mutated form of Cdc25C, in which serine 287 was replaced by an alanine (S287A), was added to cycling egg extracts, S287A accelerated entry into M-phase. Furthermore, the addition of S287A overcame the G 2 arrest caused by p42MAPK, driving the extract into M-phase. p90 Rsk a kinase that is the target of p42MAPK, was phosphorylated and activated (pp90 Rsk ) in the G 2 -arrested egg extracts, and was able to phosphorylate WT but not S287A in vitro. 14-3-3 proteins were associated with endogenous Cdc25C in G 2 -arrested extracts. Cdc25C(WT) that had been phosphorylated by pp90 Rsk bound 14-3-3ζ, whereas S287A could not. These data suggest that the link between the p42MAPK signaling pathway and Cdc25C involves the activation of pp90 Rsk and its phosphorylation of Cdc25C at S287, causing the binding of 14-3-3 proteins. We propose that the binding of 14-3-3 proteins to pp90 Rsk phosphorylated-Cdc25C results in a G 2 arrest in a manner similar to the cell cycle delays induced by differentiation signals that occur later in embryonic development.

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Role of the FGF and MEK signaling pathway in the ascidian embryo

Cited by 89 publications

References 62 publications

Ciona intestinalis: Chordate development made simple

Ciona intestinalis: Chordate development made simple

Cell fate polarization in ascidian mesenchyme/muscle precursors by directed FGF signaling and role for an additional ectodermal FGF antagonizing signal in notochord/nerve cord precursors

Phosphorylation of Cdc25C by pp90Rsk Contributes to a G2 Cell Cycle Arrest in Xenopus Cycling Egg Extracts

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