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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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univin expression is independent of BicC function.Double fluorescent in situ hybridization staining with univin (A, E) and foxA (B, F) in a BicC morphant (A–D) and control (E–H). (C, D) Merged image of (A) and (B). (G, H) Merged image of (E) and (F).
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f5: univin expression is independent of BicC function.Double fluorescent in situ hybridization staining with univin (A, E) and foxA (B, F) in a BicC morphant (A–D) and control (E–H). (C, D) Merged image of (A) and (B). (G, H) Merged image of (E) and (F).

Mentions: Based on these data, BicC morphants lose the differentiated anterior neurogenic ectoderm and endomesoderm. Next, we explored what happens on the lateral ectoderm (ectoderm except for anterior neurogenic ectoderm). We employed in situ hybridization to detect univin, which is initially expressed in the entire region and lateral ectoderm marker after cleavage stages25. Intriguingly, the expression pattern of univin in BicC morphants is invariant to that of control embryos (Fig. 5A–H). The size of the univin-absent area at the anterior end is almost identical between morphants and controls (Fig. 5A, E). This finding indicates that some molecular mechanisms suppressing univin expression are maintained without BicC function. Additionally, the mechanisms might be the same or related to those inducing foxQ2 expression at the anterior end of the embryo.


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)

univin expression is independent of BicC function.Double fluorescent in situ hybridization staining with univin (A, E) and foxA (B, F) in a BicC morphant (A–D) and control (E–H). (C, D) Merged image of (A) and (B). (G, H) Merged image of (E) and (F).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f5: univin expression is independent of BicC function.Double fluorescent in situ hybridization staining with univin (A, E) and foxA (B, F) in a BicC morphant (A–D) and control (E–H). (C, D) Merged image of (A) and (B). (G, H) Merged image of (E) and (F).
Mentions: Based on these data, BicC morphants lose the differentiated anterior neurogenic ectoderm and endomesoderm. Next, we explored what happens on the lateral ectoderm (ectoderm except for anterior neurogenic ectoderm). We employed in situ hybridization to detect univin, which is initially expressed in the entire region and lateral ectoderm marker after cleavage stages25. Intriguingly, the expression pattern of univin in BicC morphants is invariant to that of control embryos (Fig. 5A–H). The size of the univin-absent area at the anterior end is almost identical between morphants and controls (Fig. 5A, E). This finding indicates that some molecular mechanisms suppressing univin expression are maintained without BicC function. Additionally, the mechanisms might be the same or related to those inducing foxQ2 expression at the anterior end of the embryo.

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