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

Kim, Gil Jung; Kumano, Gaku; Nishida, Hiroki

doi:10.1242/dev.02825

Cited by 38 publications

(30 citation statements)

References 39 publications

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“…In the anterior marginal region (A6.2 and A6.4; notochord/nerve cord mother cells), FoxA and Zic transcription factors act as competence factors within the signal-receiving cells (Kumano et al, 2006). The daughter cell that receives the FGF signal (A7.3 and A7.7) becomes the notochord precursor and the one that does not (A7.4 and A7.8) adopts a nerve cord fate, which is the default fate in the anterior marginal region (Nakatani et al, 1996;Minokawa et al, 2001;Kim et al, 2007). In the posterior region, mesenchyme/ muscle mother cells (B6.2) of 32-cell embryos divide asymmetrically into mesenchyme (B7.3) and muscle (B7.4) daughter cells.…”

Section: Cell Fate Change In Relation To the Number Of Cell Division mentioning

confidence: 99%

Tissue-specific regulation of the number of cell division rounds by inductive cell interaction and transcription factors during ascidian embryogenesis

Fujikawa

Takatori

Kuwajima

et al. 2011

Developmental Biology

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Mechanisms that regulate the number of cells constituting the body have remained largely elusive. We approached this issue in the ascidian, Halocynthia roretzi, which develops into a tadpole larva with a small number of cells. The embryonic cells divide 11 times on average from fertilization to hatching. The number of cell division rounds varies among tissue types. For example, notochord cells divide 9 times and give rise to large postmitotic cells in the tadpole. The number of cell division rounds in partial embryos derived from tissue-precursor blastomeres isolated at the 64-cell stage also varied between tissues and coincided with their counterparts in the intact whole embryos to some extent, suggesting tissue-autonomous regulation of cell division. Manipulation of cell fates in notochord, nerve cord, muscle, and mesenchyme lineage cells by inhibition or ectopic activation of the inductive FGF signal changed the number of cell divisions according to the altered fate. Knockdown and missexpression of Brachyury (Bra), an FGF-induced notochord-specific key transcription factor for notochord differentiation, indicated that Bra is also responsible for regulation of the number of cell division rounds, suggesting that Bra activates a putative mechanism to halt cell division at a specific stage. The outcome of precocious expression of Bra suggests that the mechanism involves a putative developmental clock that is likely shared in blastomeres other than those of notochord and functions to terminate cell division at three rounds after the 64-cell stage. Precocious expression of Bra has no effect on progression of the developmental clock itself.

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Section: Cell Fate Change In Relation To the Number Of Cell Division mentioning

confidence: 99%

Tissue-specific regulation of the number of cell division rounds by inductive cell interaction and transcription factors during ascidian embryogenesis

Fujikawa

Takatori

Kuwajima

et al. 2011

Developmental Biology

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“…It is probably important to isolate cDNA of the intracellular transport-related genes and to analyze roles of FGF signaling in the polarized distribution of mitochondria. FGF signaling promotes mesenchyme/notochord fates and suppresses muscle/nerve cord fate during ascidian embryogenesis (Kim et al, 2007). Thus, there is a possibility that FGF signaling involved in regulation of the differential segregation of mitochondria.…”

Section: Resultsmentioning

confidence: 99%

Mitochondria-Specific Monoclonal Antibodies in Eggs and Embryos of the Ascidian Halocynthia roretzi

2017

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Ascidian embryos have become an important model for embryological studies, offering a simple example for mechanisms of cytoplasmic components segregation. It is a well-known example that the asymmetric segregation of mitochondria into muscle lineage cells occurs during ascidian embryogenesis. However, it is still unclear which signaling pathway is involved in this process. To obtain molecular markers for studying mechanisms involved in the asymmetric distribution of mitochondria, we have produced monoclonal antibodies, Mito-1, Mito-2 and Mito-3, that specifically recognize mitochondriarich cytoplasm in cells of the ascidian Halocynthia roretzi embryos. These antibodies stained cytoplasm like reticular structure in epidermis cells, except for nuclei, at the early tailbud stage. Similar pattern was observed in vital staining of mitochondria with DiOC2, a fluorescent probe of mitochondria. Immunostaining with these antibodies showed that mitochondria are evenly distributed in the animal hemisphere blastomeres at cleavage stages, whereas not in the vegetal hemisphere blastomeres. Mitochondria were transferred to the presumptive muscle and nerve cord lineage cells of the marginal zone in the vegetal hemisphere more than to the presumptive mesenchyme, notochord and endoderm lineage of the central zone. Therefore, it is suggested that these antibodies will be useful markers for studying mechanisms involved in the polarized distribution of mitochondria during ascidian embryogenesis.

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“…The signal is ephrin in Ciona intestinalis (Picco et al, 2007). The antagonistic signal, which is also likely to be ephrin in Halocynthia, redundantly functions to prevent nerve cord cells from being induced to notochord by blocking a component of the FGF signal pathway: MAPK activation (Kim et al, 2007;Picco et al, 2007). Consistently, when the animal hemisphere was removed from FoxB-knockdown embryos, ectopic Bra expression was observed in most cases.…”

Section: Research Articlementioning

confidence: 87%

“…The FGF signal from endoderm blastomeres also induces a mesenchyme fate in the posterior region of the vegetal hemisphere at the same stage as notochord induction (Kim and Nishida, 2001;Kim et al, 2007). Similar to notochord induction, temporal decay of competence for mesenchyme induction was observed during the 64-cell stage (Kim et al, 2000).…”

Section: Loss Of Competence To Respond To the Fgf Signal During Mesenmentioning

confidence: 98%

“…Development 138 (12) Previous studies have shown that an antagonistic signal from the animal hemisphere inhibits nerve cord precursor cells from expressing Bra before FoxB expression in nerve cord precursor cells (Kim et al, 2007). It is possible that the antagonistic signal lasts even beyond the 64-cell stage and prevents nerve cord cells from expressing Bra.…”

Section: Research Articlementioning

confidence: 99%

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The transcription factor FoxB mediates temporal loss of cellular competence for notochord induction in ascidian embryos

et al. 2011

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In embryos of the ascidian Halocynthia roretzi, the competence of isolated presumptive notochord blastomeres to respond to fibroblast growth factor (FGF) for induction of the primary notochord decays by 1 hour after cleavage from the 32- to 64-cell stage. This study analyzes the molecular mechanisms responsible for this loss of competence and provides evidence for a novel mechanism. A forkhead family transcription factor, FoxB, plays a role in competence decay by preventing the induction of notochord-specific Brachyury (Bra) gene expression by the FGF/MAPK signaling pathway. Unlike the mechanisms reported previously in other animals, no component in the FGF signal transduction cascade appeared to be lost or inactivated at the time of competence loss. Knockdown of FoxB functions allowed the isolated cells to retain their competence for a longer period, and to respond to FGF with expression of Bra beyond the stage at which competence was normally lost. FoxB acts as a transcription repressor by directly binding to the cis-regulatory element of the Bra gene. Our results suggest that FoxB prevents ectopic induction of the notochord fate within the cells that assume a default nerve cord fate, after the stage when notochord induction has been completed. The merit of this system is that embryos can use the same FGF signaling cascade again for another purpose in the same cell lineage at later stages by keeping the signaling cascade itself available. Temporally and spatially regulated FoxB expression in nerve cord cells was promoted by the ZicN transcription factor and absence of FGF/MAPK signaling.

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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

Cited by 38 publications

References 39 publications

Tissue-specific regulation of the number of cell division rounds by inductive cell interaction and transcription factors during ascidian embryogenesis

Tissue-specific regulation of the number of cell division rounds by inductive cell interaction and transcription factors during ascidian embryogenesis

Mitochondria-Specific Monoclonal Antibodies in Eggs and Embryos of the Ascidian Halocynthia roretzi

The transcription factor FoxB mediates temporal loss of cellular competence for notochord induction in ascidian embryos

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