Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Electronic Gene Ontology annotations created by transferring manual GO annotations between related proteins based on shared sequence features
Combined Automated Annotation using Multiple IEA Methods
SpSoxB1, a maternally encoded transcription factor asymmetrically distributed among early sea urchin blastomeres.
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Discovery of the SpSoxB1 cDNA (the Q9Y0D7 sequence); maternal mRNA is uniform, protein is nuclear in all early blastomeres and is lost from micromere nuclei at fourth cleavage.
"SpSoxB1 maternal transcripts are uniformly distributed in the unfertilized egg and the protein accumulates to similar, high concentrations in all nuclei of 4- and 8-cell embryos. However, at fourth cleavage, the micromeres, which are partitioned by asymmetric division of the vegetal 4 blastomeres, have reduced nuclear levels of the protein, while high levels persist in their sister macromeres and in the mesomeres."
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Nuclear SoxB1 becomes confined to ectoderm; it is the earliest spatially restricted transcriptional regulator on the animal-vegetal axis.
"The vegetal region lacking nuclear SpSoxB1 gradually expands so that, after blastula stage, only cells in differentiating ectoderm accumulate this protein in their nuclei."
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SpSoxB1 binds the Sox cis element of the SpAN promoter in EMSA and the nuclear-extract complex is supershifted by anti-SpSoxB1 antiserum.
"In vitro translated SpSoxB1 forms a specific complex with this cis element whose mobility is identical to that formed by a protein in nuclear extracts. An anti-SpSoxB1 rabbit polyclonal antiserum specifically supershifts this DNA-protein complex"
SpSoxB1 serves an essential architectural function in the promoter SpAN, a tolloid/BMP1-related gene.
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The SpSoxB1 site is essential for SpAN promoter activity in vivo (20-fold), but multimerised Sox sites cannot activate a basal promoter.
"Here we show that multimerized SpSoxB1 elements cannot activate transcription from the SpAN basal promoter in vivo."
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SpSoxB1 strongly bends DNA and is proposed to act architecturally at SpAN.
"The results described above suggest a model in which SpSoxB1 promotes transcription of the SpAN gene primarily through DNA bending, rather than through transcriptional activation."
Tight regulation of SpSoxB factors is required for patterning and morphogenesis in sea urchin embryos.
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SpSoxB1 overexpression animalises the embryo, phenocopying loss of nuclear beta-catenin; the effect is DNA-binding independent.
"Suppression of vegetal fates involves interference at the protein-protein level because a mutation of SpSoxB1 that prevents its binding to DNA does not significantly reduce this activity."
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SoxB1 loss of function elevates TCF/beta-catenin reporter output in vivo.
"Reduction in SpSoxB1 level results in elevated TCF/Lef-beta-catenin-dependent expression of a luciferase reporter gene in vivo, indicating that in the normal embryo this protein suppresses the primary vegetal signaling mechanism that is required for specification of mesenchyme and endoderm."
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Normal SoxB1 is nevertheless required for gastrulation and endoderm differentiation (treated here as an indirect requirement).
"Surprisingly, normal expression of SpSoxB1 is required for gastrulation and endoderm differentiation, as shown by both morpholino-mediated translational interference and expression of a dominant negative protein."
SoxB1 downregulation in vegetal lineages of sea urchin embryos is achieved by both transcriptional repression and selective protein turnover.
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SoxB1 is cleared from vegetal lineages by beta-catenin-dependent protein turnover that can be activated by Pmar1.
"We show that SoxB1 is regulated at the level of protein turnover in these lineages. This mechanism is dependent on nuclear beta-catenin function. It can be activated by Pmar1, but not by Krl, both of which function downstream of beta-catenin/TCF-Lef."
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In mesomeres SoxB1 is subject to negative autoregulation.
"However, in mesomeres, SoxB1 appears to be subject to negative autoregulation that helps to maintain tight regulation of SoxB1 mRNA levels in presumptive ectoderm."
SpKrl: a direct target of beta-catenin regulation required for endoderm differentiation in sea urchin embryos.
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SpKrl (Blimp1/Krox), a direct beta-catenin/TCF target, represses soxb1 transcription in vegetal cells.
"SpKrl negatively regulates expression of the animalizing transcription factor, SpSoxB1."
Global regulatory logic for specification of an embryonic cell lineage.
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Absence of nuclear SoxB1 is one of the initial micromere-specific character states in the skeletogenic GRN, and SoxB1 is regarded as an antagonist of beta-catenin cofactor function.
"SoxB1 is believed to act as an antagonist of the transcriptional cofactor function of β-catenin."
Cis-regulatory analysis of nodal and maternal control of dorsal-ventral axis formation by Univin, a TGF-beta related to Vg1.
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SoxB1 (with Tcf and Univin) is essential for nodal expression; the nodal 5' module carries Sox sites.
"This work shows that Tcf, SoxB1 and Univin play essential roles in the regulation of nodal expression in the sea urchin and suggests that some of the regulatory interactions controlling nodal expression predate the chordates."
Geometric control of ciliated band regulatory states in the sea urchin embryo.
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soxb1 morpholino downregulates nearly all ciliated-band and ectoderm regulatory genes; SoxB1 is a pan-ectodermal activator with negative autoregulation and repression of otx beta1/2.
"Remarkably, almost all of the regulatory genes specifically expressed within these domains are downregulated by interference with SoxB1 expression, implying their common activation by this factor."
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SoxB1 is described as a pan-ectodermal transcription factor.
"SoxB1 is a pan-ectodermal transcription factor that is known to affect many other regulatory genes of the oral and aboral ectoderm GRNs"
Direct development of neurons within foregut endoderm of sea urchin embryos.
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SoxB1 marks uncommitted neural precursors and is eliminated from differentiating neurons in ectoderm and foregut.
"Just as these factors disappear when neurons differentiate in mouse embryos, so also is SoxB1 eliminated from differentiating neurons in ectoderm and foregut endoderm in sea urchin embryos."
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Persistent foregut SoxB1 is proposed to preserve neural potential by antagonising canonical Wnt signaling.
"We propose that SoxB1 function supports retention of pluripotency in this region, at least in part by antagonizing canonical Wnt signaling that drives endomesoderm development."
Neurogenesis in the sea urchin embryo is initiated uniquely in three domains.
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soxb1 is expressed in all three neurogenic territories, and its knockdown alters proneural gene expression territory-specifically.
"Expression of the six proneural transcription factors shows that the response to knockdown of soxC , sip1 or soxb1 differs when the three territories are compared"