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bicaudal-C is required for the formation of anterior neurogenic ectoderm in the sea urchin embryo.

Yaguchi S, Yaguchi J, Inaba K - Sci Rep (2014)

Bottom Line: Loss-of-function experiments reveal that BicC is required for serotonergic neurogenesis and for expression of ankAT-1 gene, which is essential for the formation of apical tuft cilia in the neurogenic ectoderm of the sea urchin embryo.In contrast, the expression of FoxQ2, the neurogenic ectoderm specification transcription factor, is invariant in BicC morphants.Because FoxQ2 is an upstream factor of serotonergic neurogenesis and ankAT-1 expression, these data indicate that BicC functions in regulating the events that are coordinated by FoxQ2 during sea urchin embryogenesis.

View Article: PubMed Central - PubMed

Affiliation: 1] Shimoda Marine Research Center, University of Tsukuba, 5-10-1 Shimoda, Shizuoka 415-0025, Japan [2] Japanese Association for Marine Biology (JAMBIO).

ABSTRACT
bicaudal-C (bicC) mRNA encodes a protein containing RNA-binding domains that is reported to be maternally present with deflection in the oocytes/eggs of some species. The translated protein plays a critical role in the regulation of cell fate specification along the body axis during early embryogenesis in flies and frogs. However, it is unclear how it functions in eggs in which bicC mRNA is uniformly distributed, for instance, sea urchin eggs. Here, we show the function of BicC in the formation of neurogenic ectoderm of the sea urchin embryo. Loss-of-function experiments reveal that BicC is required for serotonergic neurogenesis and for expression of ankAT-1 gene, which is essential for the formation of apical tuft cilia in the neurogenic ectoderm of the sea urchin embryo. In contrast, the expression of FoxQ2, the neurogenic ectoderm specification transcription factor, is invariant in BicC morphants. Because FoxQ2 is an upstream factor of serotonergic neurogenesis and ankAT-1 expression, these data indicate that BicC functions in regulating the events that are coordinated by FoxQ2 during sea urchin embryogenesis.

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The expression pattern of bicC during sea urchin embryogenesis.Maternal bicC mRNA was detected at the unfertilized egg (A), 16-cell (B, C) and cleavage stages (D). Fluorescent in situ hybridization with DAPI staining was performed on a 16-cell embryo (C), cleavage stage (D), mesenchyme blastula (MBL; E), and early gastrula (eG; H). The signal was missing in MBL (E, F). bicC was expressed at the vegetal plate of eG (G, H), mid-gastrula (mG; I) and late gastrula (lG; J). In prism larva, bicC was expressed at the ciliary band and the tip of gut (K, L). The bar in (A) is 20 μm.
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f1: The expression pattern of bicC during sea urchin embryogenesis.Maternal bicC mRNA was detected at the unfertilized egg (A), 16-cell (B, C) and cleavage stages (D). Fluorescent in situ hybridization with DAPI staining was performed on a 16-cell embryo (C), cleavage stage (D), mesenchyme blastula (MBL; E), and early gastrula (eG; H). The signal was missing in MBL (E, F). bicC was expressed at the vegetal plate of eG (G, H), mid-gastrula (mG; I) and late gastrula (lG; J). In prism larva, bicC was expressed at the ciliary band and the tip of gut (K, L). The bar in (A) is 20 μm.

Mentions: To investigate the bicC spatial pattern during embryogenesis, we employed in situ hybridization using bicC RNA-probe. As previously reported15, bicC mRNA is maternally expressed and ubiquitously detected until the cleavage stage and is almost absent at the blastula stages (Fig. 1A–F). Fluorescent in situ hybridization using a tyramide amplification system16 under the same microscopic conditions shows that the gene is ubiquitously expressed during the early stages and is almost completely absent at the blastula stage (Fig. 1C–E). When gastrulation is initiated, the vegetal plate cells begin to express bicC mRNA (Fig. 1G, H). The vegetal plate expression is maintained (Fig. 1I, J), but expression is not detected in the invaginated gut cells until the late gastrula stage. The expression pattern becomes complicated in the prism stage. The vegetal plate expression is diminished as foregut expression begins. Moreover, in the ciliary band, a few cells express the gene at the lateral and ventral regions (Fig. 1K, L). These complex and dynamic patterns of bicC mRNA localization suggest that the gene expression is regulated by multiple inputs during sea urchin development.


bicaudal-C is required for the formation of anterior neurogenic ectoderm in the sea urchin embryo.

Yaguchi S, Yaguchi J, Inaba K - Sci Rep (2014)

The expression pattern of bicC during sea urchin embryogenesis.Maternal bicC mRNA was detected at the unfertilized egg (A), 16-cell (B, C) and cleavage stages (D). Fluorescent in situ hybridization with DAPI staining was performed on a 16-cell embryo (C), cleavage stage (D), mesenchyme blastula (MBL; E), and early gastrula (eG; H). The signal was missing in MBL (E, F). bicC was expressed at the vegetal plate of eG (G, H), mid-gastrula (mG; I) and late gastrula (lG; J). In prism larva, bicC was expressed at the ciliary band and the tip of gut (K, L). The bar in (A) is 20 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4215294&req=5

f1: The expression pattern of bicC during sea urchin embryogenesis.Maternal bicC mRNA was detected at the unfertilized egg (A), 16-cell (B, C) and cleavage stages (D). Fluorescent in situ hybridization with DAPI staining was performed on a 16-cell embryo (C), cleavage stage (D), mesenchyme blastula (MBL; E), and early gastrula (eG; H). The signal was missing in MBL (E, F). bicC was expressed at the vegetal plate of eG (G, H), mid-gastrula (mG; I) and late gastrula (lG; J). In prism larva, bicC was expressed at the ciliary band and the tip of gut (K, L). The bar in (A) is 20 μm.
Mentions: To investigate the bicC spatial pattern during embryogenesis, we employed in situ hybridization using bicC RNA-probe. As previously reported15, bicC mRNA is maternally expressed and ubiquitously detected until the cleavage stage and is almost absent at the blastula stages (Fig. 1A–F). Fluorescent in situ hybridization using a tyramide amplification system16 under the same microscopic conditions shows that the gene is ubiquitously expressed during the early stages and is almost completely absent at the blastula stage (Fig. 1C–E). When gastrulation is initiated, the vegetal plate cells begin to express bicC mRNA (Fig. 1G, H). The vegetal plate expression is maintained (Fig. 1I, J), but expression is not detected in the invaginated gut cells until the late gastrula stage. The expression pattern becomes complicated in the prism stage. The vegetal plate expression is diminished as foregut expression begins. Moreover, in the ciliary band, a few cells express the gene at the lateral and ventral regions (Fig. 1K, L). These complex and dynamic patterns of bicC mRNA localization suggest that the gene expression is regulated by multiple inputs during sea urchin development.

Bottom Line: Loss-of-function experiments reveal that BicC is required for serotonergic neurogenesis and for expression of ankAT-1 gene, which is essential for the formation of apical tuft cilia in the neurogenic ectoderm of the sea urchin embryo.In contrast, the expression of FoxQ2, the neurogenic ectoderm specification transcription factor, is invariant in BicC morphants.Because FoxQ2 is an upstream factor of serotonergic neurogenesis and ankAT-1 expression, these data indicate that BicC functions in regulating the events that are coordinated by FoxQ2 during sea urchin embryogenesis.

View Article: PubMed Central - PubMed

Affiliation: 1] Shimoda Marine Research Center, University of Tsukuba, 5-10-1 Shimoda, Shizuoka 415-0025, Japan [2] Japanese Association for Marine Biology (JAMBIO).

ABSTRACT
bicaudal-C (bicC) mRNA encodes a protein containing RNA-binding domains that is reported to be maternally present with deflection in the oocytes/eggs of some species. The translated protein plays a critical role in the regulation of cell fate specification along the body axis during early embryogenesis in flies and frogs. However, it is unclear how it functions in eggs in which bicC mRNA is uniformly distributed, for instance, sea urchin eggs. Here, we show the function of BicC in the formation of neurogenic ectoderm of the sea urchin embryo. Loss-of-function experiments reveal that BicC is required for serotonergic neurogenesis and for expression of ankAT-1 gene, which is essential for the formation of apical tuft cilia in the neurogenic ectoderm of the sea urchin embryo. In contrast, the expression of FoxQ2, the neurogenic ectoderm specification transcription factor, is invariant in BicC morphants. Because FoxQ2 is an upstream factor of serotonergic neurogenesis and ankAT-1 expression, these data indicate that BicC functions in regulating the events that are coordinated by FoxQ2 during sea urchin embryogenesis.

Show MeSH