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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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BicC is required for endoderm formation.The pmar1 gene was expressed in the BicC morphant (A) as it was in the control (B), but endo16 was not detected in BicC morphants (C, E) at the time that it was expressed in control embryos (D, F). In contrast, spatial control of foxA expression was almost invariant in the BicC morphant (G, I, K) and in the control (H, J, L).
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f4: BicC is required for endoderm formation.The pmar1 gene was expressed in the BicC morphant (A) as it was in the control (B), but endo16 was not detected in BicC morphants (C, E) at the time that it was expressed in control embryos (D, F). In contrast, spatial control of foxA expression was almost invariant in the BicC morphant (G, I, K) and in the control (H, J, L).

Mentions: At 48 hr, BicC morphants have dispersed cells at the vegetal pole but no gut formation (Fig. 3E). These dispersed cells have P4 antigen (Fig. 3B–E, G–J), indicating that they are differentiated primary mesenchyme cells (PMC)24. As expected, pmar1, an essential gene for PMC specification, is unchanged in BicC morphants compared to control embryos (Fig. 4A, B). These results indicate that the specification and differentiation of PMC, i.e., skeletogenic mesenchyme cells, are normal in BicC morphants. In contrast, endo16, an early endomesoderm and late endoderm marker, is not expressed during embryogenesis, at least, until 26 hr, without BicC (cf.Fig. 4C,E with D, F). However, foxA is expressed at the vegetal region (Fig. 4G–L), but the expression pattern is invariant until 29 hr because the endoderm never invaginates. These data suggest that some but not all aspects of endomesoderm specification occurred in BicC morphants. Although the ectoderm region is covered with oral ectoderm in the BicC morphant (Fig. 3), foxA expression is not detected around the mouth region (Fig. 4K, L). Because a mouth stomodeum is not observed even in 48 hr morphants (Fig. 3E), the morphants do not form a mouth structure without proper BicC function.


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)

BicC is required for endoderm formation.The pmar1 gene was expressed in the BicC morphant (A) as it was in the control (B), but endo16 was not detected in BicC morphants (C, E) at the time that it was expressed in control embryos (D, F). In contrast, spatial control of foxA expression was almost invariant in the BicC morphant (G, I, K) and in the control (H, J, L).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: BicC is required for endoderm formation.The pmar1 gene was expressed in the BicC morphant (A) as it was in the control (B), but endo16 was not detected in BicC morphants (C, E) at the time that it was expressed in control embryos (D, F). In contrast, spatial control of foxA expression was almost invariant in the BicC morphant (G, I, K) and in the control (H, J, L).
Mentions: At 48 hr, BicC morphants have dispersed cells at the vegetal pole but no gut formation (Fig. 3E). These dispersed cells have P4 antigen (Fig. 3B–E, G–J), indicating that they are differentiated primary mesenchyme cells (PMC)24. As expected, pmar1, an essential gene for PMC specification, is unchanged in BicC morphants compared to control embryos (Fig. 4A, B). These results indicate that the specification and differentiation of PMC, i.e., skeletogenic mesenchyme cells, are normal in BicC morphants. In contrast, endo16, an early endomesoderm and late endoderm marker, is not expressed during embryogenesis, at least, until 26 hr, without BicC (cf.Fig. 4C,E with D, F). However, foxA is expressed at the vegetal region (Fig. 4G–L), but the expression pattern is invariant until 29 hr because the endoderm never invaginates. These data suggest that some but not all aspects of endomesoderm specification occurred in BicC morphants. Although the ectoderm region is covered with oral ectoderm in the BicC morphant (Fig. 3), foxA expression is not detected around the mouth region (Fig. 4K, L). Because a mouth stomodeum is not observed even in 48 hr morphants (Fig. 3E), the morphants do not form a mouth structure without proper BicC function.

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