Two histospecific enzyme expressions in the same cleavage‐arrested one‐celled ascidian embryos

Whittaker, Jonathan; Meedel, Thomas H.

doi:10.1002/jez.1402500208

Cited by 65 publications

(31 citation statements)

References 23 publications

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“…The reaction deposits a purple product, as described previously (Whittaker and Meedel, 1989). Formation of notochord was monitored by staining with the Not-1 monoclonal antibody.…”

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

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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.

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“…The reaction deposits a purple product, as described previously (Whittaker and Meedel, 1989). Formation of notochord was monitored by staining with the Not-1 monoclonal antibody.…”

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

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“…The differentiation of endoderm cells in experimental embryos was monitored by the histochemical detection of alkaline phosphatase as previously described (Whittaker and Meedel, 1989).…”

Section: Detection Of Differentiation Markersmentioning

confidence: 99%

A Twist-like bHLH gene is a downstream factor of an endogenous FGF and determines mesenchymal fate in the ascidian embryos

2003

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Ascidian larvae develop mesenchyme cells in their trunk. A fibroblast growth factor (FGF9/16/20) is essential and sufficient for induction of the mesenchyme in Ciona savignyi. We have identified two basic helix-loop-helix (bHLH) genes named Twist-like1 and Twist-like2 as downstream factors of this FGF. These two genes are phylogenetically closely related to each other, and were expressed specifically in the mesenchymal cells after the 110-cell stage. Gene-knockdown experiments using a specific morpholino oligonucleotide demonstrated that Twist-like1 plays an essential role in determination of the mesenchyme and that Twist-like2 is a downstream factor of Twist-like1. In addition, both overexpression and misexpression of Twist-like1 converts non-mesenchymal cells to mesenchymal cells.We also demonstrate that the upstream regulatory mechanisms of Twist-like1 are different between B-line mesenchymal cells and the A-line mesenchymal cells called `trunk lateral cells'. FGF9/16/20 is required for the expression of Twist-like1 in B-line mesenchymal precursor cells, whereas FGF, FoxD and another novel bHLH factor called NoTrlc are required for Twist-like1 to be expressed in the A-line mesenchymal precursor cells. Therefore, two different but partially overlapping mechanisms are required for the expression of Twist-like1 in the mesenchymal precursors, which triggers the differentiation of the mesenchyme in Ciona embryos.

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“…Differentiation of endoderm was monitored by histochemical detection of alkaline phosphatase (ALP) activity using the method described by Whittaker and Meedel (1989) with 5-bromo-4-chloro-3-indolyl phosphate as the substrate. RNA probes for in situ hybridization were prepared with a digoxigenin (DIG) RNA labeling kit (Boehringer Mannheim, Mannheim, Germany).…”

Section: Detection Of Tissue-specific Markersmentioning

confidence: 99%

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

2001

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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.

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Two histospecific enzyme expressions in the same cleavage‐arrested one‐celled ascidian embryos

Cited by 65 publications

References 23 publications

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

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

A Twist-like bHLH gene is a downstream factor of an endogenous FGF and determines mesenchymal fate in the ascidian embryos

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

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