Induction of Notochord during Ascidian Embryogenesis

Nakatani, Yuki; Nishida, Hiroki

doi:10.1006/dbio.1994.1315

Cited by 122 publications

(80 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, when treatment was started approximately 20 min after formation of the A7.3 notochord precursor blastomeres, most embryos expressed the Not-1 antigen. These results coincide well with those of previous studies that involved blastomere recombination and bFGF treatment at various stages (Nakatani & Nishida 1994;Nakatani et al 1996). In normal development, the notochord precursors acquire the ability to develop autonomously at the early 64-cell stage.…”

Section: Notochord Induction and Fgf Signalingsupporting

confidence: 93%

“…Previous reports have shown that inductive interactions are required for notochord and mesenchyme specification and that an FGF-like signal is involved in these processes (Nakatani & Nishida 1994;Nakatani et al 1996;Kim & Nishida 1999;Kim et al 2000). However, it remained to be elucidated whether an endogenous FGF signal is indeed involved in these processes, because all of these studies used human recombinant bFGF.…”

Section: Signaling By Fgf In Notochord and Mesenchyme Inductionmentioning

confidence: 99%

See 1 more Smart Citation

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

2001

Self Cite

View full text Add to dashboard Cite

In the ascidian embryo, a fibroblast growth factor (FGF)-like signal from presumptive endoderm blastomeres between the 32-cell and early 64-cell stages induces the formation of notochord and mesenchyme cells. However, it has not been known whether endogenous FGF signaling is involved in the process. Here it is shown that 64-cell embryos exhibit a marked increase in endogenous extracellular signal-regulated kinase (ERK/MAPK) activity. The increase in ERK activity was reduced by treatment with an FGF receptor 1 inhibitor, SU5402, and a MEK (ERK kinase/MAPKK) inhibitor, U0126. Both drugs blocked the formation of notochord and mesenchyme when embryos were treated at the 32-cell stage, but not at the 2-or 110-cell stages. The dominant-negative form of Ras also suppressed notochord and mesenchyme formation. Both inhibitors suppressed induction by exogenous basic FGF. These results suggest that the FGF signaling cascade is indeed necessary for the formation of notochord and mesenchyme cells during ascidian embryogenesis. It is also shown that FGF signaling is required for formation of the secondary notochord, secondary muscle and neural tissues, and at least ERK activity is necessary for the formation of trunk lateral cells and posterior endoderm. Therefore, FGF and MEK signaling are required for the formation of various tissues in the ascidian embryo.

show abstract

Section: Notochord Induction and Fgf Signalingsupporting

confidence: 93%

Section: Signaling By Fgf In Notochord and Mesenchyme Inductionmentioning

confidence: 99%

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

2001

Self Cite

View full text Add to dashboard Cite

show abstract

“…Experimental manipulations have demonstrated that specification of the primary notochord lineage of ascidians requires inductive signals from vegetal blastomeres fated to become endoderm (Nakatani and Nishida, 1994). This requirement seems to be similar to the inductive specification of mesoderm by vegetal cells in amphibians (Nieuwkoop, 1969).…”

Section: Larval Tissues Notochordmentioning

confidence: 92%

Ciona intestinalis: Chordate development made simple

2005

View full text Add to dashboard Cite

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.

show abstract

“…Formation of notochord was monitored by staining with the Not-1 monoclonal antibody. It recognizes a notochordspecific antigen at the middle tail bud stage (Nishikata and Satoh, 1990;Nakatani and Nishida, 1994). The monoclonal antibody Mch-3 was used for monitoring mesenchyme formation.…”

Section: Monitoring Of Tissue Formation and Inhibition Of Cell Divisionmentioning

confidence: 99%

Nuclear accumulation of β‐catenin and transcription of downstream genes are regulated by zygotic Wnt5α and maternal Dsh in ascidian embryos

Kawai¹,

Iida²,

Kumano³

et al. 2007

Developmental Dynamics

Self Cite

View full text Add to dashboard Cite

Nuclear ␤-catenin plays crucial roles in the establishment of the embryonic axis and formation of mesendoderm tissues in ascidians and other animals. However, the cue responsible for nuclear accumulation of ␤-catenin in the vegetal hemisphere is still unknown in ascidians. Here, we investigated the roles of Wnt5␣ and Dsh in the nuclear accumulation of ␤-catenin and activation of its downstream genes in the ascidian Halocynthia roretzi. Wnt5␣ knockdown embryos lost nuclear accumulation of ␤-catenin at the 64-cell stage but not at the 32-cell stage, and expression of Hr-lim, one of the targets of ␤-catenin, was impaired in the anterior region of the embryo. Zygotic Wnt5␣ expression in the anterior-vegetal blastomeres was primarily responsible for these defects. Dsh knockdown showed no effect on nuclear localization of ␤-catenin, but inhibited Hr-lim expression in the posterior region. These results suggest that maintenance of nuclear Hr-␤-catenin after the 64-cell stage is regulated by zygotic Hr-Wnt5␣, and that expression of its target genes is modulated by both Hr-Wnt5␣ and Hr-Dsh. Our results also highlight the importance of nuclear accumulation of ␤-catenin up to the 32-cell stage through a still unclarified mechanism. Developmental Dynamics 236:1570 -1582, 2007.

show abstract

Induction of Notochord during Ascidian Embryogenesis

Cited by 122 publications

References 0 publications

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

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

Ciona intestinalis: Chordate development made simple

Nuclear accumulation of β‐catenin and transcription of downstream genes are regulated by zygotic Wnt5α and maternal Dsh in ascidian embryos

Contact Info

Product

Resources

About