Sox9b is one of two zebrafish co-orthologs of vertebrate SOX9, produced by the teleost-specific genome duplication. It is an SRY-related HMG-box (SoxE group) transcription factor whose HMG box is nearly identical to that of Sox9a and human SOX9 and binds the Sox consensus DNA motif; it acts in the nucleus to activate target genes such as col2a1a and col11a2. Sox9b is expressed in pharyngeal endoderm and epithelia, subsets of craniofacial and pectoral cartilage, otic placode, retina, heart myocardium, the hepatopancreatic, intrahepatic and intrapancreatic ducts including pancreatic centroacinar progenitor cells, and adult oocytes. It is needed for proper chondrocyte numbers in a subset of craniofacial cartilages, and it has roles that zebrafish sox9a does not share: development of the pancreaticobiliary ductal system, maintenance of Notch signalling in biliary cells, restraint of endocrine differentiation from ductal progenitors downstream of Notch and retinoic acid signalling, liver regeneration by biliary transdifferentiation, retinal differentiation, and proepicardium, epicardium and heart valve formation. It acts partly redundantly with sox9a in otic development.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0000122 negative regulation of transcription by RNA polymerase II | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: IBA: negative regulation of transcription by RNA polymerase II (PTN000741645, human SOX9 donor). Reason: SOX9 represses some targets in mammals and the HMG box is conserved in Sox9b (file:DANRE/sox9a/sox9a-bioinformatics/RESULTS.md). In zebrafish, Sox9b is part of a Runx3-Egr1-Sox9b cascade that represses fsta in pharyngeal endoderm, though direct repression by Sox9b is not shown. Kept as an inherited, non-core property. Supporting Evidence: PMID:23209659 the endodermal factors Runx3 and Sox9b form a regulatory cascade with Egr1 resulting in transcriptional repression of the fsta gene, encoding a BMP antagonist, in pharyngeal endoderm. |
| GO:0000978 RNA polymerase II cis-regulatory region sequence-specific DNA binding | IBA GO_REF:0000033 | ACCEPT | Summary: IBA: RNA polymerase II cis-regulatory region sequence-specific DNA binding. Reason: Sox9b binds HMG consensus DNA in vitro; its HMG box is 98.6% identical to Sox9a and human SOX9. Supporting Evidence: PMID:11180959 Both Sox9a and Sox9b proteins bind to the HMG consensus DNA sequences in vitro. PMID:19210963 After the sox9 gene duplication event, regulatory elements controlling the expression of sox9 co-orthologs apparently partitioned in a tissue-specific fashion, but the Sox9 proteins encoded by sox9a and sox9b retained the ability to regulate col11a2, presumably by binding to regulatory sites for the col11a2 gene. |
| GO:0000981 DNA-binding transcription factor activity, RNA polymerase II-specific | IBA GO_REF:0000033 | ACCEPT | Summary: IBA: DNA-binding transcription factor activity, RNA polymerase II-specific. Reason: Core molecular function: DNA binding plus a mapped transactivation domain, and loss of sox9b reduces expression of Sox9 target genes such as col11a2 in the cartilages it is expressed in. Supporting Evidence: PMID:11180959 Both Sox9a and Sox9b proteins bind to the HMG consensus DNA sequences in vitro. PMID:11180959 We tested different domains for transactivation potential and identified a potential activation domain located in the middle of both Sox9a and Sox9b. PMID:19210963 col11a2 expression was greatly reduced in the mandibular and ceratohyal cartilages in sox9b mutants, but was retained in the ethmoid plate and trabeculae of the neurocranium |
| GO:0002009 morphogenesis of an epithelium | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: IBA: morphogenesis of an epithelium (donors include both zebrafish sox9a and sox9b). Reason: Well supported for Sox9b, which is required for morphogenesis of the intrahepatic, intrapancreatic and hepatopancreatic ductal epithelia and contributes to otic epithelium formation; kept as a broad, non-core term. Supporting Evidence: PMID:22537488 All these observations reveal that sox9b is required not only for the morphogenesis of the IHD but also for morphogenesis and differentiation of the IPD and HPD system. PMID:12668634 These cells fail to form if sox9b function is also blocked. |
| GO:0002062 chondrocyte differentiation | IBA GO_REF:0000033 | ACCEPT | Summary: IBA: chondrocyte differentiation. Reason: Sox9b is required for proper chondrocyte numbers and col2a1/col11a2 expression in a subset of craniofacial cartilages; together with sox9a it is required for all cartilage. Supporting Evidence: PMID:15689370 Chondrocytes failed to stack in sox9a mutants, failed to attain proper numbers in sox9b mutants and failed in both morphogenetic processes in double mutants. PMID:23209659 while in zebrafish both sox9a and sox9b are required for col2a1 expression. PMID:19210963 col11a2 expression was greatly reduced in the mandibular and ceratohyal cartilages in sox9b mutants, but was retained in the ethmoid plate and trabeculae of the neurocranium |
| GO:0003170 heart valve development | IMP PMID:23775563 Sox9b is required for epicardium formation and plays a role ... | KEEP AS NON CORE | Summary: IMP: heart valve development (sox9b morpholino). Reason: Sox9b morphants and mutants fail to form valve cushions and leaflets. This is a copy-specific role: sox9a knockdown had no cardiac effect. Supporting Evidence: PMID:23775563 Fish lacking sox9b failed to form valve cushions and leaflets. PMID:23775563 Knock down of sox9a expression did not cause cardiac malformations, or defects in epicardium development. |
| GO:0003309 type B pancreatic cell differentiation | IMP PMID:27565026 Sox9b is a mediator of retinoic acid signaling restricting e... | KEEP AS NON CORE | Summary: IMP: type B pancreatic cell differentiation (transgenic dominant-negative/overexpression genotype). Reason: Sox9b acts in ductal centroacinar progenitors to restrain their differentiation into endocrine (including beta) cells downstream of Notch and retinoic acid signalling; loss of Sox9b activity depletes the progenitor pool. The acts_upstream_of_or_within relation accommodates this negative, progenitor-level role. Non-core. Supporting Evidence: PMID:27565026 Blocking Sox9b activity either in sox9bfh313 homozygous mutant fish or by over expression of truncated sox9b results in fewer CAC progenitors available to produce new endocrine cells PMID:27565026 Importantly, Sox9b activity is necessary and sufficient for RA signaling to impart this effect. |
| GO:0003342 proepicardium development | IMP PMID:23775563 Sox9b is required for epicardium formation and plays a role ... | KEEP AS NON CORE | Summary: IMP: proepicardium development. Reason: Loss of sox9b prevents formation of the proepicardium and epicardium. Sox9b is expressed in ventricular myocardium but not in the proepicardium itself, and cardiomyocyte-restricted dominant-negative Sox9b disrupts cardiac morphogenesis, so the effect on the proepicardium is likely non-cell-autonomous; acts_upstream_of_or_within is appropriate. Copy-specific. Supporting Evidence: PMID:23775563 Loss of sox9b prevented the formation of epicardium progenitors comprising the proepicardium on the pericardial wall, and prevented the formation and migration of the epicardial layer around the heart. PMID:23775563 Furthermore, sox9b is required for PE, epicardium, and valve formation. PMID:23775563 Furthermore, while sox9b expression was critical for the formation of the epicardium, we found sox9b expressed in ventricular cardiomyocytes but not in cells of the PE or epicardium. PMID:30224706 We generated a dominant-negative sox9b (dnsox9b) to inhibit sox9b target gene expression and used the Gal4/UAS system to drive dnsox9b specifically in cardiomyocytes. |
| GO:0003342 proepicardium development | IMP PMID:23775563 Sox9b is required for epicardium formation and plays a role ... | KEEP AS NON CORE | Summary: IMP: proepicardium development. Reason: Loss of sox9b prevents formation of the proepicardium and epicardium. Sox9b is expressed in ventricular myocardium but not in the proepicardium itself, and cardiomyocyte-restricted dominant-negative Sox9b disrupts cardiac morphogenesis, so the effect on the proepicardium is likely non-cell-autonomous; acts_upstream_of_or_within is appropriate. Copy-specific. Supporting Evidence: PMID:23775563 Loss of sox9b prevented the formation of epicardium progenitors comprising the proepicardium on the pericardial wall, and prevented the formation and migration of the epicardial layer around the heart. PMID:23775563 Furthermore, while sox9b expression was critical for the formation of the epicardium, we found sox9b expressed in ventricular cardiomyocytes but not in cells of the PE or epicardium. PMID:30224706 We generated a dominant-negative sox9b (dnsox9b) to inhibit sox9b target gene expression and used the Gal4/UAS system to drive dnsox9b specifically in cardiomyocytes. |
| GO:0003677 DNA binding | IEA GO_REF:0000104 | ACCEPT | Summary: IEA (UniRule): DNA binding. Reason: Correct, general. Supporting Evidence: PMID:11180959 Both Sox9a and Sox9b proteins bind to the HMG consensus DNA sequences in vitro. |
| GO:0005634 nucleus | IBA GO_REF:0000033 | ACCEPT | Summary: IBA: nucleus (is_active_in). Reason: Sox9b immunostaining co-localizes with nuclear markers in pancreatic centroacinar cells; consistent with its transcription-factor function. Supporting Evidence: PMID:27565026 As can be seen in Figure 6A, Sox9b co-localized to nuclear mCherry within CACs. |
| GO:0005634 nucleus | IEA GO_REF:0000120 | ACCEPT | Summary: IEA: nucleus. Reason: Consistent with direct observation. Supporting Evidence: PMID:27565026 As can be seen in Figure 6A, Sox9b co-localized to nuclear mCherry within CACs. |
| GO:0007507 heart development | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: IBA: heart development (sox9b itself among donors). Reason: Sox9b has experimental support for proepicardium, epicardium and valve development, so it is correctly inside the clade inheriting this function; the zebrafish cardiac role is held by sox9b, not sox9a (see the sox9a review). Supporting Evidence: PMID:23775563 Furthermore, sox9b is required for PE, epicardium, and valve formation. PMID:23775563 Knock down of sox9a expression did not cause cardiac malformations, or defects in epicardium development. PMID:30224706 We generated a dominant-negative sox9b (dnsox9b) to inhibit sox9b target gene expression and used the Gal4/UAS system to drive dnsox9b specifically in cardiomyocytes. PMID:30224706 Thus, indicating that the truncated sox9b variant is able to act as a dominant negative as predicted and significantly reduce sox9b-mediated transcription. |
| GO:0030318 melanocyte differentiation | IMP PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | UNDECIDED | Summary: IMP: melanocyte differentiation (Yan et al. 2005, sox9b b971 genotype). Reason: Only the abstract is cached and it does not describe a pigment-cell phenotype, although it reports that sox9 regulates the early neural crest genes foxd3 and sox10. The curator likely used the full text, which could not be accessed. Also, the b971 allele deletes sox9b together with sox8 and other genes, so a pigment phenotype may not be attributable to sox9b alone. Not removed; left undecided. Supporting Evidence: PMID:15689370 sox9 helps regulate other early crest genes, including foxd3, sox10, snai1b and crestin, as well as the cartilage gene col2a1 and the bone gene runx2a PMID:22719264 the chromosomal deletion which underlies the b971 lesion removes eleven other genes, greatly limiting the use of this allele to study the function of Sox9b. |
| GO:0030916 otic vesicle formation | IGI PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | KEEP AS NON CORE | Summary: IGI: otic vesicle formation (sox9a;sox9b double mutant). Reason: Ears are reduced in each single mutant and mostly absent in double mutants: shared, partly redundant function with sox9a. Supporting Evidence: PMID:15689370 Ears are somewhat reduced in each single mutant but are mostly absent in the double mutant. |
| GO:0031016 pancreas development | IMP PMID:22537488 Zebrafish sox9b is crucial for hepatopancreatic duct develop... | ACCEPT | Summary: IMP: pancreas development (sox9b fh313). Reason: Copy-specific core role: Sox9b is required for morphogenesis and differentiation of the intrapancreatic and hepatopancreatic ducts and for duct-derived endocrine cells; sox9a is not expressed in the digestive organs. Supporting Evidence: PMID:22537488 All these observations reveal that sox9b is required not only for the morphogenesis of the IHD but also for morphogenesis and differentiation of the IPD and HPD system. PMID:22537488 Finally, we show that sox9b is essential for endocrine cell formation from the pancreatic ducts and for beta cell regeneration. PMID:22719264 As in wild-type, sox9a expression appears to be excluded from the digestive organs in sox9bfh313 mutants, suggesting that sox9a expression does not compensate for the reduction of Sox9b function in these mutants. |
| GO:0031016 pancreas development | IMP PMID:22719264 Sox9b is a key regulator of pancreaticobiliary ductal system... | ACCEPT | Summary: IMP: pancreas development (sox9b fh313). Reason: As above; independent study with the same nonsense allele. Supporting Evidence: PMID:22719264 Altogether, these data indicate that Sox9b function is required for the development of the intrapancreatic ductal system as well as - directly or indirectly - for the formation of secondary islets. PMID:22719264 Strikingly, sox9b(fh313) homozygous mutants survive to adulthood and exhibit cholestasis associated with hepatic and pancreatic duct proliferation, cyst formation, and fibrosis. |
| GO:0031018 endocrine pancreas development | IMP PMID:27565026 Sox9b is a mediator of retinoic acid signaling restricting e... | KEEP AS NON CORE | Summary: IMP: endocrine pancreas development (transgenic Sox9b gain/loss of function). Reason: Sox9b controls the number of ductal centroacinar progenitors and restrains their endocrine differentiation; secondary islet formation depends on it. Supported; non-core relative to its ductal morphogenesis role. Supporting Evidence: PMID:27565026 Blocking Sox9b activity either in sox9bfh313 homozygous mutant fish or by over expression of truncated sox9b results in fewer CAC progenitors available to produce new endocrine cells PMID:22719264 Altogether, these data indicate that Sox9b function is required for the development of the intrapancreatic ductal system as well as - directly or indirectly - for the formation of secondary islets. |
| GO:0031018 endocrine pancreas development | IMP PMID:27565026 Sox9b is a mediator of retinoic acid signaling restricting e... | KEEP AS NON CORE | Summary: IMP: endocrine pancreas development (transgenic Sox9b gain/loss of function). Reason: Sox9b controls the number of ductal centroacinar progenitors and restrains their endocrine differentiation; secondary islet formation depends on it. Supported; non-core relative to its ductal morphogenesis role. Supporting Evidence: PMID:27565026 Blocking Sox9b activity either in sox9bfh313 homozygous mutant fish or by over expression of truncated sox9b results in fewer CAC progenitors available to produce new endocrine cells PMID:22719264 Altogether, these data indicate that Sox9b function is required for the development of the intrapancreatic ductal system as well as - directly or indirectly - for the formation of secondary islets. |
| GO:0031099 regeneration | IMP PMID:24315993 Regeneration of liver after extreme hepatocyte loss occurs m... | MODIFY | Summary: IMP: regeneration (biliary transdifferentiation after hepatocyte ablation). Reason: The term is very general. The study concerns liver regeneration after extreme hepatocyte loss, which requires Notch signalling and Sox9b activation in cholangiocytes. GO:0097421 liver regeneration is the appropriate, more specific term. Full text not cached; the abstract supports this. Proposed replacements: liver regeneration Supporting Evidence: PMID:24315993 this process required Notch signaling and, in turn, activation of Sox9b in cholangiocytes. |
| GO:0032332 positive regulation of chondrocyte differentiation | IBA GO_REF:0000033 | ACCEPT | Summary: IBA: positive regulation of chondrocyte differentiation. Reason: Consistent with Sox9b promotion of chondrocyte differentiation and target gene expression in the cartilages it is expressed in. Supporting Evidence: PMID:15689370 Chondrocytes failed to stack in sox9a mutants, failed to attain proper numbers in sox9b mutants and failed in both morphogenetic processes in double mutants. PMID:23209659 while in zebrafish both sox9a and sox9b are required for col2a1 expression. |
| GO:0035118 embryonic pectoral fin morphogenesis | IMP PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | KEEP AS NON CORE | Summary: IMP: embryonic pectoral fin morphogenesis (sox9b mutant/morphants). Reason: Each co-ortholog is expressed in and required for a distinct subset of the pectoral appendage. Supporting Evidence: PMID:15689370 Distinct subsets of the craniofacial skeleton, otic placode and pectoral appendage express each gene, and are defective in each single mutant. |
| GO:0035118 embryonic pectoral fin morphogenesis | IMP PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | KEEP AS NON CORE | Summary: IMP: embryonic pectoral fin morphogenesis (sox9b mutant/morphants). Reason: Each co-ortholog is expressed in and required for a distinct subset of the pectoral appendage. Supporting Evidence: PMID:15689370 Distinct subsets of the craniofacial skeleton, otic placode and pectoral appendage express each gene, and are defective in each single mutant. |
| GO:0043049 otic placode formation | IGI PMID:12668634 Fgf3 and Fgf8 dependent and independent transcription factor... | KEEP AS NON CORE | Summary: IGI: otic placode formation (combined loss with Df(b380)). Reason: Residual otic cells in embryos lacking dlx3b, dlx4b and sox9a fail to form when sox9b is also blocked; unlike sox9a, sox9b expression is Fgf3/8-independent. Supporting Evidence: PMID:12668634 Removal of dlx3b, dlx4b and sox9a genes together also blocks ear development, although a few residual cells form an otic epithelium. PMID:12668634 These cells fail to form if sox9b function is also blocked. PMID:12668634 Expression of sox9a but not dlx3b, dlx4b or sox9b requires Fgf3 and Fgf8. |
| GO:0043049 otic placode formation | IMP PMID:12668634 Fgf3 and Fgf8 dependent and independent transcription factor... | KEEP AS NON CORE | Summary: IMP: otic placode formation. Reason: As above. Supporting Evidence: PMID:12668634 These cells fail to form if sox9b function is also blocked. |
| GO:0048709 oligodendrocyte differentiation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: IBA: oligodendrocyte differentiation (PTN002910118; zebrafish donor sox9a). Reason: Sox9b is expressed with sox9a in hindbrain rhombomere-centre glial progenitor domains, and residual glial marker expression in sox9a mutants is attributed to sox9b, but sox9b loss has not been tested directly for gliogenesis (its mutant has excess CNS apoptosis). The IBA is plausible and there is no evidence of loss; kept as non-core. Supporting Evidence: PMID:20023158 although sox9a was delayed relative to sox9b , both genes were expressed in rhombomere centres PMID:20023158 residual expression of glial markers in these mutants is probably due to the sox9b co-orthologue, which has an overlapping expression profile. |
| GO:0048839 inner ear development | IGI PMID:19132125 A zebrafish model for Waardenburg syndrome type IV reveals d... | KEEP AS NON CORE | Summary: IGI: inner ear development (with sox10 mutant). Reason: Group E sox genes, including sox9b, act redundantly in otic patterning. Supporting Evidence: PMID:19132125 they act redundantly to maintain sox10 expression throughout otic tissue and to restrict fgf8 expression to anterior macula regions |
| GO:0048839 inner ear development | IMP PMID:19132125 A zebrafish model for Waardenburg syndrome type IV reveals d... | KEEP AS NON CORE | Summary: IMP: inner ear development (morpholinos). Reason: As above. Supporting Evidence: PMID:19132125 they act redundantly to maintain sox10 expression throughout otic tissue and to restrict fgf8 expression to anterior macula regions |
| GO:0050935 iridophore differentiation | IMP PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | UNDECIDED | Summary: IMP: iridophore differentiation (Yan et al. 2005, sox9b b971 genotype). Reason: As for melanocyte differentiation: the cached abstract does not describe the pigment phenotype, and the b971 deletion removes sox8 and other genes as well as sox9b. Full text needed. Supporting Evidence: PMID:15689370 sox9 helps regulate other early crest genes, including foxd3, sox10, snai1b and crestin, as well as the cartilage gene col2a1 and the bone gene runx2a PMID:19210963 The b971 mutant allele of sox9b used in this study deletes sox9b and some surrounding genes including sox8 |
| GO:0051216 cartilage development | IMP PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | ACCEPT | Summary: IMP: cartilage development (sox9b b971 mutant). Reason: Sox9b is required for normal chondrocyte numbers in a subset of craniofacial cartilages; col11a2 is lost from mandibular and ceratohyal cartilage in sox9b mutants. Caveats: b971 is a multi-gene deletion (morpholino phenocopy supports attribution to sox9b), and a later study (Lin et al. 2021, Aquaculture and Fisheries, no PMID; known here only via the deep-research summary) reported grossly normal cartilage in CRISPR sox9b frameshift mutants. That discrepancy may reflect genetic compensation in PTC alleles, the extra genes deleted in b971, or a subtler phenotype (chondrocyte number) not scored in gross staining; it does not override the curated IMP. Supporting Evidence: PMID:15689370 Chondrocytes failed to stack in sox9a mutants, failed to attain proper numbers in sox9b mutants and failed in both morphogenetic processes in double mutants. PMID:15689370 Distinct subsets of the craniofacial skeleton, otic placode and pectoral appendage express each gene, and are defective in each single mutant. PMID:19210963 col11a2 expression was greatly reduced in the mandibular and ceratohyal cartilages in sox9b mutants, but was retained in the ethmoid plate and trabeculae of the neurocranium file:DANRE/sox9b/sox9b-deep-research-falcon.md CRISPR *sox9b* Ξ11 and Ξ20 alleles deleting the HMG and Q/S domains produced grossly normal maxillary, mandibular, and pectoral-fin cartilage, whereas *sox9a* mutants had misshapen pectoral fins and lacked scapulocoracoid cartilage. |
| GO:0051216 cartilage development | IMP PMID:15689370 A pair of Sox: distinct and overlapping functions of zebrafi... | ACCEPT | Summary: IMP: cartilage development (sox9b morpholinos). Reason: Morpholino knockdown phenocopies the mutant cartilage defects; reduced sox9b expression also underlies TCDD-induced jaw malformation. Supporting Evidence: PMID:15689370 Chondrocytes failed to stack in sox9a mutants, failed to attain proper numbers in sox9b mutants and failed in both morphogenetic processes in double mutants. PMID:18784347 Sox9b, a critical chondrogenic transcription factor, was the most significantly reduced transcript in the jaw. |
| GO:0060021 roof of mouth development | IMP PMID:22052544 Sox9 is upstream of microRNA-140 in cartilage. | KEEP AS NON CORE | Summary: IMP: roof of mouth development (sox9b mutant palate). Reason: sox9b mutants have malformed small palates, a consequence of its chondrogenic role in anterior neurocranial cartilage. Supporting Evidence: PMID:22052544 mutation of Sox9b reduces cartilage development, especially having malformed small palates |
| GO:0060041 retina development in camera-type eye | IMP PMID:19210963 Expression profiling of zebrafish sox9 mutants reveals that ... | KEEP AS NON CORE | Summary: IMP: retina development in camera-type eye. Reason: sox9b mutants have smaller eyes and lose retinal expression of neurod, crx, vsx1 and calb2a/b, whereas sox9a mutant retinas are normal: a copy-specific role. Supporting Evidence: PMID:19210963 Considering the expression pattern of sox9b, the expression of candidate genes in sox9b mutants, and the phenotype observed in the retina of sox9b mutants, we conclude that sox9b is essential for retinal development. PMID:19210963 In contrast, sox9a mutant retinas had no obvious defects, even though sox9a is expressed in the inner nuclear layer at 68 hpf |
| GO:0061008 hepaticobiliary system development | IMP PMID:22719264 Sox9b is a key regulator of pancreaticobiliary ductal system... | ACCEPT | Summary: IMP: hepaticobiliary system development (sox9b fh313). Reason: Copy-specific core role: Sox9b is required for morphogenesis of the hepatopancreatic ductal system and intrahepatic biliary network; mutants develop cholestasis, duct cysts and fibrosis. Supporting Evidence: PMID:22719264 Strikingly, sox9b(fh313) homozygous mutants survive to adulthood and exhibit cholestasis associated with hepatic and pancreatic duct proliferation, cyst formation, and fibrosis. PMID:22719264 Altogether, these data indicate that Sox9b is required for the maintenance but not the initiation of Notch signaling in the intrahepatic biliary cells. PMID:22537488 All these observations reveal that sox9b is required not only for the morphogenesis of the IHD but also for morphogenesis and differentiation of the IPD and HPD system. |
| GO:0061032 visceral serous pericardium development | IMP PMID:23775563 Sox9b is required for epicardium formation and plays a role ... | KEEP AS NON CORE | Summary: IMP: visceral serous pericardium development (epicardium). Reason: Loss of sox9b prevents formation and migration of the epicardial layer; copy-specific cardiac role. Supporting Evidence: PMID:23775563 Loss of sox9b prevented the formation of epicardium progenitors comprising the proepicardium on the pericardial wall, and prevented the formation and migration of the epicardial layer around the heart. |
| GO:0061032 visceral serous pericardium development | IMP PMID:23775563 Sox9b is required for epicardium formation and plays a role ... | KEEP AS NON CORE | Summary: IMP: visceral serous pericardium development (epicardium). Reason: Loss of sox9b prevents formation and migration of the epicardial layer; copy-specific cardiac role. Supporting Evidence: PMID:23775563 Loss of sox9b prevented the formation of epicardium progenitors comprising the proepicardium on the pericardial wall, and prevented the formation and migration of the epicardial layer around the heart. |
| GO:0001228 DNA-binding transcription activator activity, RNA polymerase II-specific | IDA PMID:11180959 Two sox9 genes on duplicated zebrafish chromosomes: expressi... | NEW | Summary: Proposed: Sox9b is a sequence-specific transcriptional activator. Reason: Chiang et al. 2001 showed that both zebrafish Sox9 proteins bind HMG consensus DNA and mapped a transactivation domain in the middle of each; both proteins retain the ability to regulate the Sox9 target col11a2. Proposed identically for sox9a so that the shared molecular function is annotated consistently across the pair. Supporting Evidence: PMID:11180959 Both Sox9a and Sox9b proteins bind to the HMG consensus DNA sequences in vitro. PMID:11180959 We tested different domains for transactivation potential and identified a potential activation domain located in the middle of both Sox9a and Sox9b. PMID:19210963 After the sox9 gene duplication event, regulatory elements controlling the expression of sox9 co-orthologs apparently partitioned in a tissue-specific fashion, but the Sox9 proteins encoded by sox9a and sox9b retained the ability to regulate col11a2, presumably by binding to regulatory sites for the col11a2 gene. |
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Download this section (compressed HTML)Q: Are the cartilage, pigment and otic phenotypes originally attributed to the sox9b b971 deletion reproduced by sox9b point or frameshift alleles, given that b971 also removes sox8 and other genes?
Q: Would Sox9a protein rescue sox9b-specific ductal, retinal and cardiac phenotypes if expressed from sox9b regulatory elements?
Q: Why do CRISPR sox9b frameshift mutants reportedly have grossly normal cartilage while b971 deletion mutants and morphants do not: transcriptional adaptation (e.g. sox9a or sox8 upregulation), the extra genes removed by b971, or morpholino off-target effects?
Experiment: Knock sox9a coding sequence into the sox9b locus and assay pancreaticobiliary duct, retina and epicardium, to test whether copy-specific roles are due only to expression partition.
Experiment: Analyse pigment-cell (melanophore, iridophore) phenotypes in sox9b fh313 homozygotes to resolve whether the b971-based pigment annotations reflect sox9b.
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