Multiple endocrine defects in adult-onset Sprouty1/2/4 triple knockout mice

Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play distinct and overlapping roles in embryo morphogenesis and are considered to be tumor suppressors in adult life. Genetic experiments in mice have de...

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Published inScientific reports Vol. 14; no. 1; pp. 19479 - 10
Main Authors Altés, Gisela, Olomí, Anna, Perramon-Güell, Aida, Hernández, Sara, Casanovas, Anna, Pérez, Aurora, Díaz-Tocados, Juan Miguel, Valdivielso, José Manuel, Megino, Cristina, Navaridas, Raúl, Matias-Guiu, Xavier, Klein, Ophir D., Egea, Joaquim, Dolcet, Xavi, Yeramian, Andrée, Encinas, Mario
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 22.08.2024
Nature Publishing Group
Nature Portfolio
Subjects
631/1647
631/443
631/45
692/163
Adaptor Proteins, Signal Transducing - genetics
Animals
Body weight gain
Embryogenesis
Embryonic growth stage
Endocrine System Diseases - genetics
Endocrine System Diseases - metabolism
Eyelid
Female
Fibroblast Growth Factor-23
Food intake
Humanities and Social Sciences
Hyperthyroidism
Hypophosphatemia
Intracellular Signaling Peptides and Proteins - genetics
Kinases
Male
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mice, Knockout
Morphogenesis
multidisciplinary
Nerve Tissue Proteins
Phosphaturia
Phosphoproteins - genetics
Phosphoproteins - metabolism
Protein Serine-Threonine Kinases
Receptor mechanisms
Science
Science (multidisciplinary)
Tumorigenesis
Online AccessGet full text

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Abstract Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play distinct and overlapping roles in embryo morphogenesis and are considered to be tumor suppressors in adult life. Genetic experiments in mice have defined in great detail the role of these genes during embryonic development, however their function in adult mice is less clearly established. Here we generate adult-onset, whole body Spry1/2/4 triple knockout mice. Tumor incidence in triple mutant mice is comparable to that of wild type littermates of up to one year of age, indicating that Sprouty loss per se is not sufficient to initiate tumorigenesis. On the other hand, triple knockout mice do not gain weight as they age, show less visceral fat, and have lower plasma glucose levels than wild type littermates, despite showing similar food intake and slightly reduced motor function. They also show alopecia, eyelid inflammation, and mild hyperthyroidism. Finally, triple knockout mice present phosphaturia and hypophosphatemia, suggesting exacerbated signaling downstream of FGF23. In conclusion, triple knockout mice develop a series of endocrine abnormalities but do not show increased tumor incidence.
AbstractList Abstract Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play distinct and overlapping roles in embryo morphogenesis and are considered to be tumor suppressors in adult life. Genetic experiments in mice have defined in great detail the role of these genes during embryonic development, however their function in adult mice is less clearly established. Here we generate adult-onset, whole body Spry1/2/4 triple knockout mice. Tumor incidence in triple mutant mice is comparable to that of wild type littermates of up to one year of age, indicating that Sprouty loss per se is not sufficient to initiate tumorigenesis. On the other hand, triple knockout mice do not gain weight as they age, show less visceral fat, and have lower plasma glucose levels than wild type littermates, despite showing similar food intake and slightly reduced motor function. They also show alopecia, eyelid inflammation, and mild hyperthyroidism. Finally, triple knockout mice present phosphaturia and hypophosphatemia, suggesting exacerbated signaling downstream of FGF23. In conclusion, triple knockout mice develop a series of endocrine abnormalities but do not show increased tumor incidence.
Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play distinct and overlapping roles in embryo morphogenesis and are considered to be tumor suppressors in adult life. Genetic experiments in mice have defined in great detail the role of these genes during embryonic development, however their function in adult mice is less clearly established. Here we generate adult-onset, whole body Spry1/2/4 triple knockout mice. Tumor incidence in triple mutant mice is comparable to that of wild type littermates of up to one year of age, indicating that Sprouty loss per se is not sufficient to initiate tumorigenesis. On the other hand, triple knockout mice do not gain weight as they age, show less visceral fat, and have lower plasma glucose levels than wild type littermates, despite showing similar food intake and slightly reduced motor function. They also show alopecia, eyelid inflammation, and mild hyperthyroidism. Finally, triple knockout mice present phosphaturia and hypophosphatemia, suggesting exacerbated signaling downstream of FGF23. In conclusion, triple knockout mice develop a series of endocrine abnormalities but do not show increased tumor incidence.
Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play distinct and overlapping roles in embryo morphogenesis and are considered to be tumor suppressors in adult life. Genetic experiments in mice have defined in great detail the role of these genes during embryonic development, however their function in adult mice is less clearly established. Here we generate adult-onset, whole body Spry1/2/4 triple knockout mice. Tumor incidence in triple mutant mice is comparable to that of wild type littermates of up to one year of age, indicating that Sprouty loss per se is not sufficient to initiate tumorigenesis. On the other hand, triple knockout mice do not gain weight as they age, show less visceral fat, and have lower plasma glucose levels than wild type littermates, despite showing similar food intake and slightly reduced motor function. They also show alopecia, eyelid inflammation, and mild hyperthyroidism. Finally, triple knockout mice present phosphaturia and hypophosphatemia, suggesting exacerbated signaling downstream of FGF23. In conclusion, triple knockout mice develop a series of endocrine abnormalities but do not show increased tumor incidence.Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play distinct and overlapping roles in embryo morphogenesis and are considered to be tumor suppressors in adult life. Genetic experiments in mice have defined in great detail the role of these genes during embryonic development, however their function in adult mice is less clearly established. Here we generate adult-onset, whole body Spry1/2/4 triple knockout mice. Tumor incidence in triple mutant mice is comparable to that of wild type littermates of up to one year of age, indicating that Sprouty loss per se is not sufficient to initiate tumorigenesis. On the other hand, triple knockout mice do not gain weight as they age, show less visceral fat, and have lower plasma glucose levels than wild type littermates, despite showing similar food intake and slightly reduced motor function. They also show alopecia, eyelid inflammation, and mild hyperthyroidism. Finally, triple knockout mice present phosphaturia and hypophosphatemia, suggesting exacerbated signaling downstream of FGF23. In conclusion, triple knockout mice develop a series of endocrine abnormalities but do not show increased tumor incidence.
ArticleNumber 19479
Author Perramon-Güell, Aida
Díaz-Tocados, Juan Miguel
Matias-Guiu, Xavier
Valdivielso, José Manuel
Yeramian, Andrée
Encinas, Mario
Casanovas, Anna
Olomí, Anna
Megino, Cristina
Klein, Ophir D.
Egea, Joaquim
Dolcet, Xavi
Hernández, Sara
Altés, Gisela
Pérez, Aurora
Navaridas, Raúl
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  givenname: José Manuel
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  surname: Matias-Guiu
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  organization: Oncologic Pathology Group, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Department of Pathology, Hospital Universitari de Bellvitge
– sequence: 12
  givenname: Ophir D.
  surname: Klein
  fullname: Klein, Ophir D.
  organization: Program in Craniofacial Biology and Department of Orofacial Sciences, University of California, San Francisco, Department of Pediatrics, Cedars-Sinai Guerin Children’s
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  surname: Egea
  fullname: Egea, Joaquim
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  email: mario.encinas@mex.udl.cat
  organization: Developmental and Oncogenic Signaling Group, Edifici Biomedicina I, Lab 2.8, Department of Experimental Medicine, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida
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Snippet Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they play...
Abstract Genes of the Sprouty family (Spry1-4) are feedback inhibitors of receptor tyrosine kinases, especially of Ret and the FGF receptors. As such, they...
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SubjectTerms 631/1647
631/443
631/45
692/163
Adaptor Proteins, Signal Transducing - genetics
Animals
Body weight gain
Embryogenesis
Embryonic growth stage
Endocrine System Diseases - genetics
Endocrine System Diseases - metabolism
Eyelid
Female
Fibroblast Growth Factor-23
Food intake
Humanities and Social Sciences
Hyperthyroidism
Hypophosphatemia
Intracellular Signaling Peptides and Proteins - genetics
Kinases
Male
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mice
Mice, Knockout
Morphogenesis
multidisciplinary
Nerve Tissue Proteins
Phosphaturia
Phosphoproteins - genetics
Phosphoproteins - metabolism
Protein Serine-Threonine Kinases
Receptor mechanisms
Science
Science (multidisciplinary)
Tumorigenesis
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Title Multiple endocrine defects in adult-onset Sprouty1/2/4 triple knockout mice
URI https://link.springer.com/article/10.1038/s41598-024-70529-w
https://www.ncbi.nlm.nih.gov/pubmed/39174793
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