Developmental Signals - Fibroblast Growth Factor: Difference between revisions
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{{Neural crest}} cell migration during early {{chicken}} embryo development{{#pmid:30520400|PMID30520400}} | {{Neural crest}} cell migration during early {{chicken}} embryo development{{#pmid:30520400|PMID30520400}} | ||
:"Fibroblast growth factor (FGF) signalling acts as one of modulators that control neural crest cell (NCC) migration, but how this is achieved is still unclear. In this study, we investigated the effects of FGF signalling on NCC migration by blocking this process. Constructs that were capable of inducing Sprouty2 (Spry2) or dominant-negative FGFR1 (Dn-FGFR1) expression were transfected into the cells making up the neural tubes. Our results revealed that blocking FGF signalling at stage HH10 (neurulation stage) could enhance NCC migration at both the cranial and trunk levels in the developing embryos. It was established that FGF-mediated NCC migration was not due to altering the expression of N-cadherin in the neural tube. Instead, we determined that cyclin D1 was overexpressed in the cranial and trunk levels when Sprouty2 was upregulated in the dorsal neural tube. These results imply that the cell cycle was a target of FGF signalling through which it regulates NCC migration at the neurulation stage." | :"Fibroblast growth factor (FGF) signalling acts as one of modulators that control neural crest cell (NCC) migration, but how this is achieved is still unclear. In this study, we investigated the effects of FGF signalling on NCC migration by blocking this process. Constructs that were capable of inducing Sprouty2 (Spry2) or dominant-negative FGFR1 (Dn-FGFR1) expression were transfected into the cells making up the neural tubes. Our results revealed that blocking FGF signalling at stage HH10 (neurulation stage) could enhance NCC migration at both the cranial and trunk levels in the developing embryos. It was established that FGF-mediated NCC migration was not due to altering the expression of N-cadherin in the neural tube. Instead, we determined that cyclin D1 was overexpressed in the cranial and trunk levels when Sprouty2 was upregulated in the dorsal neural tube. These results imply that the cell cycle was a target of FGF signalling through which it regulates NCC migration at the neurulation stage." | ||
===Spinal Cord=== | |||
'''Differentiation and localization of interneurons in the developing spinal cord depends on DOT1L expression'''{{#pmid:32471461|PMID32471461}} | |||
"Genetic and epigenetic factors contribute to the development of the spinal cord. Failure in correct exertion of the developmental programs, including neurulation, neural tube closure and neurogenesis of the diverse spinal cord neuronal subtypes results in defects of variable severity. We here report on the histone methyltransferase Disruptor of Telomeric 1 Like (DOT1L), which mediates histone H3 lysine 79 (H3K79) methylation. Conditional inactivation of DOT1L using Wnt1-cre as driver (Dot1l-cKO) showed that DOT1L expression is essential for spinal cord neurogenesis and localization of diverse neuronal subtypes, similar to its function in the development of the cerebral cortex and cerebellum. Transcriptome analysis revealed that DOT1L deficiency favored differentiation over progenitor proliferation. Dot1l-cKO mainly decreased the numbers of dI1 interneurons expressing Lhx2. In contrast, Lhx9 expressing dI1 interneurons did not change in numbers but localized differently upon Dot1l-cKO. Similarly, loss of DOT1L affected localization but not generation of dI2, dI3, dI5, V0 and V1 interneurons. The resulting derailed interneuron patterns might be responsible for increased cell death, occurrence of which was restricted to the late developmental stage {{ME18.5}}. Together our data indicate that DOT1L is essential for subtype-specific neurogenesis, migration and localization of dorsal and ventral interneurons in the developing spinal cord, in part by regulating transcriptional activation of Lhx2." | |||
==Endoderm== | ==Endoderm== | ||
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:'''Links:''' | :'''Links:''' {{Endoderm}} | {{Chicken}} | ||
==Mesoderm== | ==Mesoderm== | ||
[[File:Model for Sprouty4 and FGF in mesoderm segmentation.jpg|400px]] | [[File:Model for Sprouty4 and FGF in mesoderm segmentation.jpg|400px]] |
Revision as of 12:53, 25 July 2020
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Introduction
Fibroblast Growth Factors (FGF) were originally identified by their ability to stimulate fibroblast cell proliferation but have a role in a growing number of different tissues development and differentiation and continue to have a role in the adult.
The first two identified factors were originally given the nomenclature of acidic or basic. We now know there to be at least 22 different human FGFs (Fgf1–Fgf23). These protein growth factors are bound by 4 different cell membrane receptors (FGFR1-4). FGFRs belong to the tyrosine kinase receptor family.
The mammalian Fgf family can be divided into the intracellular Fgf11/12/13/14 subfamily (iFGFs), the endocrine hormone-like Fgf15/21/23 subfamily (hFGFs), and the paracrine canonical Fgf subfamilies, including Fgf1/2/5, Fgf3/4/6, Fgf7/10/22, Fgf8/17/18, and Fgf9/16/20.
Factor Links: AMH | hCG | BMP | sonic hedgehog | bHLH | HOX | FGF | FOX | Hippo | LIM | Nanog | NGF | Nodal | Notch | PAX | retinoic acid | SIX | Slit2/Robo1 | SOX | TBX | TGF-beta | VEGF | WNT | Category:Molecular |
Human FGF Family
Table - Human Fibroblast Growth Factor Family FGF | ||||
Approved Symbol |
Approved Name | Previous Symbols |
Synonyms | Chromosome |
---|---|---|---|---|
FGF1 | fibroblast growth factor 1 | FGFA | "AFGF, ECGF, ECGFA, ECGFB, HBGF1, ECGF-beta, FGF-alpha, GLIO703" | 5q31.3 |
FGF2 | fibroblast growth factor 2 | FGFB | 4q28.1 | |
FGF4 | fibroblast growth factor 4 | HSTF1 | "K-FGF, HBGF-4, HST, HST-1, KFGF" | 11q13.3 |
FGF5 | fibroblast growth factor 5 | 4q21.21 | ||
FGF6 | fibroblast growth factor 6 | 12p13.32 | ||
FGF7 | fibroblast growth factor 7 | KGF | 15q21.2 | |
FGF8 | fibroblast growth factor 8 | AIGF | 10q24.32 | |
FGF9 | fibroblast growth factor 9 | 13q12.11 | ||
Links: Developmental Signals - Fibroblast Growth Factor | OMIM Fgf1 | HGNC | Bmp Family | Fgf Family | Sox Family | Tbx Family |
Human FGF Family | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Protein Properties
Human FGF
- ~150–300 amino acids
- have a conserved ~120-residue core with ~30–60% identity
Some Recent Findings
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More recent papers |
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This table allows an automated computer search of the external PubMed database using the listed "Search term" text link.
More? References | Discussion Page | Journal Searches | 2019 References | 2020 References Search term: Fibroblast Growth Factor | FGF | ERK | Fibroblast Growth Factor Receptor |
Older papers |
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These papers originally appeared in the Some Recent Findings table, but as that list grew in length have now been shuffled down to this collapsible table.
See also the Discussion Page for other references listed by year and References on this current page.
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Ectoderm
neural crest cell migration during early chicken embryo development[15]
- "Fibroblast growth factor (FGF) signalling acts as one of modulators that control neural crest cell (NCC) migration, but how this is achieved is still unclear. In this study, we investigated the effects of FGF signalling on NCC migration by blocking this process. Constructs that were capable of inducing Sprouty2 (Spry2) or dominant-negative FGFR1 (Dn-FGFR1) expression were transfected into the cells making up the neural tubes. Our results revealed that blocking FGF signalling at stage HH10 (neurulation stage) could enhance NCC migration at both the cranial and trunk levels in the developing embryos. It was established that FGF-mediated NCC migration was not due to altering the expression of N-cadherin in the neural tube. Instead, we determined that cyclin D1 was overexpressed in the cranial and trunk levels when Sprouty2 was upregulated in the dorsal neural tube. These results imply that the cell cycle was a target of FGF signalling through which it regulates NCC migration at the neurulation stage."
Spinal Cord
Differentiation and localization of interneurons in the developing spinal cord depends on DOT1L expression[16]
"Genetic and epigenetic factors contribute to the development of the spinal cord. Failure in correct exertion of the developmental programs, including neurulation, neural tube closure and neurogenesis of the diverse spinal cord neuronal subtypes results in defects of variable severity. We here report on the histone methyltransferase Disruptor of Telomeric 1 Like (DOT1L), which mediates histone H3 lysine 79 (H3K79) methylation. Conditional inactivation of DOT1L using Wnt1-cre as driver (Dot1l-cKO) showed that DOT1L expression is essential for spinal cord neurogenesis and localization of diverse neuronal subtypes, similar to its function in the development of the cerebral cortex and cerebellum. Transcriptome analysis revealed that DOT1L deficiency favored differentiation over progenitor proliferation. Dot1l-cKO mainly decreased the numbers of dI1 interneurons expressing Lhx2. In contrast, Lhx9 expressing dI1 interneurons did not change in numbers but localized differently upon Dot1l-cKO. Similarly, loss of DOT1L affected localization but not generation of dI2, dI3, dI5, V0 and V1 interneurons. The resulting derailed interneuron patterns might be responsible for increased cell death, occurrence of which was restricted to the late developmental stage E18.5. Together our data indicate that DOT1L is essential for subtype-specific neurogenesis, migration and localization of dorsal and ventral interneurons in the developing spinal cord, in part by regulating transcriptional activation of Lhx2."
Endoderm
Chicken antero-posterior endoderm patterning[17]
Mesoderm
A Putative Model for the role of Sprouty4 as a mediator that links the mouse segmentation clock to the gradient of FGF signaling.[18]
The FGF signaling may be periodically inhibited by Sprouty4, by which temporal periodicity of Notch segmentation clock may be translated to spatial periodicity of the array of somites.
- In the PSM - FGF signaling establishes a posterior-to-anterior gradient, which is involved in the positioning of presumptive somite boundaries.
- Cyclic Sprouty4
- which is controlled by the Notch segmentation clock, the mechanism of which includes negative feedback loop of Hes7,
- may inhibit the FGF signaling possibly around the anterior border of the FGF signaling positive area
- where the FGF signaling is close to its threshold.
- S - somite
- PS - presumptive somite.
- Links: somitogenesis | Axial Skeleton Development | Notch | FGF
Bone
FGF9 has been shown to induce endochondral ossification in cranial mesenchyme in the mouse model.[19]
Respiration
Lung Buds
Fibroblast growth factor 10 (FGF10) expression in mesoderm required for initial lung buds, through FGFR2IIIb transmembrane tyrosine kinase receptor protein.
Branching
Fibroblast growth factor 10 (FGF10) and sonic hedgehog (SHH) form a feedback loop for branching
- mesenchyme produced FGF10 signals to the distal epithelium to upregulate SHH expression.
- SHH then feeds back to inhibit Fgf10 expression in the adjacent mesenchyme, dividing in two the Fgf10 expression domain.
- new FGF10 signaling domains serve as two chemoattractant sources, leading to bifurcation of the epithelial tip.
Loop process mediated through FGF-activated transcription factor genes Etv4 and Etv5.[21]
- Links: respiratory
Limb
FGF soaked beads (FGF-1, FGF-2 and FGF-4) are capable of inducing additional limbs in chicken embryos.[22] A later study[23] identified the endogenous signal as Fgf-8 from initially the intermediate mesoderm and then the prelimb field ectoderm for limb initiation and outgrowth, respectively.
Hearing
- fibroblast growth factor 1 - (Fgf-1) a growth factor released from cochlea sensory epithelium which stimulates spiral ganglion neurite branching.
- fibroblast growth factor 8 - (Fgf-8) a growth factor released by inner hair cells which regulates pillar cell number, position and rate of development.
- fibroblast growth factor receptor 3 - (Fgfr-3) a tyrosine kinase receptor with a role in the commitment, differentiation and position of pillar cells in the organ of corti
- Links: hearing
Palate
Fibroblast growth factors are required during palatogenesis and are candidate genes for syndromic and nonsyndromic cleft lip and cleft palate, see the recent review.[7]
FGF7, FGF8, FGF9, FGF10, FGF18 and their receptors FGFR1, FGFR2
- Links: palate | cleft palate
Abnormalities
- FGFR1 mutation has been associated with the relatively milder form of Pfeiffer syndrome type 1.
- FGFR2 and FGFR3 have been associated with the Apert, Crouzon and Pfeiffer syndromes.
FGF10
A recent mouse knock-out study has shown a single-gene deletion of Fgf10 can generate duodenal atresia in this animal model.[24]
(A) Normal gastric, pyloric, and duodenal morphology was demonstrated by wild type embryos. Null Fgf10 embryos universally demonstrated microgastria, but duodenal morphology varied according to presence and type of DA. Null embryos provided examples of: normal continuity and morphology of the duodenum for tm1 (D) and tm2 (E); type 1 DA, tm1 (F) and tm2 (G); type 2 DA, tm1 (H) and tm2 (I); and type 3 DA, tm1 (J) and tm2 (K).
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References
- ↑ Itoh N. (2010). Hormone-like (endocrine) Fgfs: their evolutionary history and roles in development, metabolism, and disease. Cell Tissue Res. , 342, 1-11. PMID: 20730630 DOI.
- ↑ 2.0 2.1 Fongang B & Kudlicki A. (2013). The precise timeline of transcriptional regulation reveals causation in mouse somitogenesis network. BMC Dev. Biol. , 13, 42. PMID: 24304493 DOI.
- ↑ Bird AD, Croft BM, Harada M, Tang L, Zhao L, Ming Z, Bagheri-Fam S, Koopman P, Wang Z, Akita K & Harley VR. (2020). Ovotesticular disorders of sex development (DSD) in FGF9 mouse models of human synostosis syndromes. Hum. Mol. Genet. , , . PMID: 32452519 DOI.
- ↑ Kantarci H, Gou Y & Riley BB. (2020). The Warburg Effect and lactate signaling augment Fgf-MAPK to promote sensory-neural development in the otic vesicle. Elife , 9, . PMID: 32338604 DOI.
- ↑ Wong KL, Akiyama R, Bessho Y & Matsui T. (2018). ERK Activity Dynamics during Zebrafish Embryonic Development. Int J Mol Sci , 20, . PMID: 30597912 DOI.
- ↑ Row RH, Pegg A, Kinney B, Farr GH, Maves L, Lowell S, Wilson V & Martin BL. (2018). BMP and FGF signaling interact to pattern mesoderm by controlling basic helix-loop-helix transcription factor activity. Elife , 7, . PMID: 29877796 DOI.
- ↑ 7.0 7.1 Weng M, Chen Z, Xiao Q, Li R & Chen Z. (2018). A review of FGF signaling in palate development. Biomed. Pharmacother. , 103, 240-247. PMID: 29655165 DOI.
- ↑ Chan WK, Price DJ & Pratt T. (2017). FGF8 morphogen gradients are differentially regulated by heparan sulphotransferases Hs2st and Hs6st1 in the developing brain. Biol Open , 6, 1933-1942. PMID: 29158323 DOI.
- ↑ Diez Del Corral R & Morales AV. (2017). The Multiple Roles of FGF Signaling in the Developing Spinal Cord. Front Cell Dev Biol , 5, 58. PMID: 28626748 DOI.
- ↑ Atsuta Y & Takahashi Y. (2015). FGF8 coordinates tissue elongation and cell epithelialization during early kidney tubulogenesis. Development , 142, 2329-37. PMID: 26130757 DOI.
- ↑ Gredler ML, Seifert AW & Cohn MJ. (2015). Tissue-specific roles of Fgfr2 in development of the external genitalia. Development , 142, 2203-12. PMID: 26081573 DOI.
- ↑ Shifley ET, Kenny AP, Rankin SA & Zorn AM. (2012). Prolonged FGF signaling is necessary for lung and liver induction in Xenopus. BMC Dev. Biol. , 12, 27. PMID: 22988910 DOI.
- ↑ Lahti L, Saarimäki-Vire J, Rita H & Partanen J. (2011). FGF signaling gradient maintains symmetrical proliferative divisions of midbrain neuronal progenitors. Dev. Biol. , 349, 270-82. PMID: 21074523 DOI.
- ↑ Yu SR, Burkhardt M, Nowak M, Ries J, Petrásek Z, Scholpp S, Schwille P & Brand M. (2009). Fgf8 morphogen gradient forms by a source-sink mechanism with freely diffusing molecules. Nature , 461, 533-6. PMID: 19741606 DOI.
- ↑ Zhang XT, Wang G, Li Y, Chuai M, Lee KKH & Yang X. (2018). Role of FGF signalling in neural crest cell migration during early chick embryo development. Zygote , , 1-8. PMID: 30520400 DOI.
- ↑ Gray de Cristoforis A, Ferrari F, Clotman F & Vogel T. (2020). Differentiation and localization of interneurons in the developing spinal cord depends on DOT1L expression. Mol Brain , 13, 85. PMID: 32471461 DOI.
- ↑ Bayha E, Jørgensen MC, Serup P & Grapin-Botton A. (2009). Retinoic acid signaling organizes endodermal organ specification along the entire antero-posterior axis. PLoS ONE , 4, e5845. PMID: 19516907 DOI.
- ↑ Hayashi S, Shimoda T, Nakajima M, Tsukada Y, Sakumura Y, Dale JK, Maroto M, Kohno K, Matsui T & Bessho Y. (2009). Sprouty4, an FGF inhibitor, displays cyclic gene expression under the control of the notch segmentation clock in the mouse PSM. PLoS ONE , 4, e5603. PMID: 19440349 DOI.
- ↑ Govindarajan V & Overbeek PA. (2006). FGF9 can induce endochondral ossification in cranial mesenchyme. BMC Dev. Biol. , 6, 7. PMID: 16504022 DOI.
- ↑ Cardoso WV & Kotton DN. (2008). Specification and patterning of the respiratory system. , , . PMID: 20614584 DOI.
- ↑ Herriges JC, Verheyden JM, Zhang Z, Sui P, Zhang Y, Anderson MJ, Swing DA, Zhang Y, Lewandoski M & Sun X. (2015). FGF-Regulated ETV Transcription Factors Control FGF-SHH Feedback Loop in Lung Branching. Dev. Cell , 35, 322-32. PMID: 26555052 DOI.
- ↑ Cohn MJ, Izpisúa-Belmonte JC, Abud H, Heath JK & Tickle C. (1995). Fibroblast growth factors induce additional limb development from the flank of chick embryos. Cell , 80, 739-46. PMID: 7889567
- ↑ Vogel A, Rodriguez C & Izpisúa-Belmonte JC. (1996). Involvement of FGF-8 in initiation, outgrowth and patterning of the vertebrate limb. Development , 122, 1737-50. PMID: 8674413
- ↑ 24.0 24.1 Teague WJ, Jones MLM, Hawkey L, Smyth IM, Catubig A, King SK, Sarila G, Li R & Hutson JM. (2018). FGF10 and the Mystery of Duodenal Atresia in Humans. Front Genet , 9, 530. PMID: 30473704 DOI.
Reviews
Articles
Su N, Xu X, Li C, He Q, Zhao L, Li C, Chen S, Luo F, Yi L, Du X, Huang H, Deng C & Chen L. (2010). Generation of Fgfr3 conditional knockout mice. Int. J. Biol. Sci. , 6, 327-32. PMID: 20582225
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Cite this page: Hill, M.A. (2024, June 8) Embryology Developmental Signals - Fibroblast Growth Factor. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Developmental_Signals_-_Fibroblast_Growth_Factor
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