Comparative integromics on BMP/GDF family
Open accessAbstract
WNT, Notch, FGF, Hedgehog and BMP signaling pathways network together during embryogenesis, tissue regeneration, and carcinogenesis. BMP2, BMP3, BMP4, BMP5, BMP6, BMP7, BMP8A, BMP8B, BMP10, BMP15, AMH, GDF1, GDF2, GDF3, GDF5, GDF6, GDF7, GDF8, GDF9, GDF10, GDF11, and GDF15 are BMP/GDF family genes within the human genome; however, transcriptional regulation of BMP/GDF family members by the canonical WNT signaling pathway remains unclear. We searched for the TCF/LEF-binding site within the promoter region of BMP/GDF family genes by using bioinformatics and human intelligence. Because four TCF/LEF-binding sites were identified within human GDF10 promoter, comparative genomics analyses on GDF10 orthologs were further performed. Chimpanzee GDF10 gene, encoding a 477-amino-acid protein, was identified within NW_112875.1 genome sequence. AY412135.1 was not the correct coding sequence for chimpanzee GDF10. Chimpanzee GDF10 showed 99.2%, 83.2% and 47.4% total amino-acid identity with human GDF10, mouse Gdf10 and human BMP3, respectively. RASGEF1A-GDF10-PRKG1 locus at human chromosome 10q11 and BMP3-PRKG2-RASGEF1B locus at human chromosome 4q21 were paralogous regions with insertions/deletions and recombination. Human GDF10 mRNA was expressed in fetal cochlea, fetal lung, testis, retina, pineal gland, other neural tissues, head and neck tumors, while mouse Gdf10 mRNA was expressed in fetal liver, inner ear, cerebellum, other neural tissues, prostate and blood vessels. Four TCF/LEF-binding sites in human GDF10 promoter were conserved in chimpanzee GDF10 promoter, but not in the mouse Gdf10 promoter; however, another TCF/LEF-binding site occurred in mouse Gdf10 promoter. Four bHLH-binding sites in human GDF10 promoter were conserved in chimpanzee GDF10 promoter, but only one in mouse Gdf10 promoter. Primate GDF10 promoters were divergent from mouse Gdf10 promoter. Because GDF10 was characterized as a potential target of canonical WNT signaling pathway in neural tissues, GDF10 is one of the targets of systems medicine, especially in the field of regenerative medicine.
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Compared to other GDFs, GDF10 has a unique gene structure.
“Compared to other GDFs, GDF10 has a unique gene structure12”
From GDF10 is a signal for axonal sprouting and functional recovery after stroke (2015) · cites this paper as [12]
The Identification of the chimpanzee GDF10 gene section describes its three-exon structure, and the Discussion describes features of the GDF10 promoter. Neither section establishes that GDF10’s gene structure is unique compared with other GDFs; the paper’s promoter comparison is mainly among GDF10 orthologs. (LLM, conf=0.78)
Experimental — accuracy not yet measuredGDF10 is a divergent member of the bone morphogenetic protein (BMP)/transforming growth factor-β (TGFβ) superfamily.
“GDF10 is a divergent member of the bone morphogenetic protein (BMP)/transforming growth factor-β (TGFβ) superfamily11–14”
From GDF10 is a signal for axonal sprouting and functional recovery after stroke (2015) · cites this paper as [12]
The Abstract identifies GDF10 as a BMP/GDF family gene, and the Discussion describes its conserved C-terminal TGFβ-like domain. The paper does not characterize GDF10 itself as a divergent member of the superfamily; its statement about divergence concerns primate versus mouse GDF10 promoters. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThough TGF and GDF10 both signal through TGFβRI/II, their signaling levels are not equivalent.
“Though TGF and GDF10 both signal through TGFβRI/II12–14, we show that their signaling levels are not equivalent.”
From GDF10 is a signal for axonal sprouting and functional recovery after stroke (2015) · cites this paper as [12]
The Introduction (page unavailable) says TGFβ-group and BMP/GDF-group signals pass through type I and type II receptors, which supports the general receptor-class point. It does not say that TGFβ and GDF10 use the same specific TGFβRI/II receptors. The statement about unequal signaling levels is presented as the citing authors’ own finding, not as a claim attributed to this source. (LLM, conf=0.78)
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- Authors
- Katoh, Y., & Katoh, M.
- Affiliations
- National Cancer Center Research Institute (JP)
- ORCID
- Katoh, Masaru
- Venue
- International Journal of Molecular Medicine
- Publisher
- Spandidos Publications
- Published
- 2006-05-01
- Volume
- 17
- Issue
- 5
- Pages
- 951-5
- ISSN
- 1107-3756 (ISSN-L)
- 1791-244X
- OpenAlex
- W2069439580
- Cited by
- 49
- References
- 26
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 1 · 2022: 2 · 2020: 5 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 4
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Keywords
- GDF10, BMP signaling, Wnt signaling, promoter analysis, comparative genomics, orthologs, transcriptional regulation, tissue-specific gene expression, paralogous loci, PRKG1
- MeSH terms
- Amino Acid Sequence, Animals, Base Composition, Base Sequence, Binding Sites, Pan troglodytes, Multigene Family, Humans, Male, Molecular Sequence Data, Phylogeny, Promoter Regions, Genetic, RNA, Messenger, Sequence Alignment, Sequence Homology, Amino Acid, Computational Biology, Bone Morphogenetic Proteins, Gene Expression Profiling, Genomics, Mice, TCF Transcription Factors, Bone Morphogenetic Protein 3, Growth Differentiation Factor 10
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