ArticleBioarchitecture
Fibroblast growth factor receptor 3 regulates microtubule formation and cell surface mechanical properties in the developing organ of Corti.
Article in Bioarchitecture. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Bioinformatic analysis reveals the potential association of ESRP1 with the splicing of cytoskeleton-associated genes in doxorubicin-resistant MCF7 breast cancer cells.Discover oncology · 2026Article
- Brain-Specific Angiogenesis Inhibitor 3 Is Expressed in the Cochlea and Is Necessary for Hearing Function in Mice.International journal of molecular sciences · 2023Article
- Thyroxine Regulates the Opening of the Organ of Corti through Affecting P-Cadherin and Acetylated Microtubule.International journal of molecular sciences · 2022Article
- Prognostic Gene Expression Signature for Age-Related Hearing Loss.Frontiers in medicine · 2022Article
- CMV-induced embryonic mouse organ of corti dysplasia: Network architecture of dysfunctional lateral inhibition.Birth defects research. Part A, Clinical and molecular teratology · 2015Article
- Nanomechanics of vascular endothelium.Cell and tissue research · 2014Review
- Inner ear supporting cells: rethinking the silent majority.Seminars in cell & developmental biology · 2013Review
- Thyroid hormone increases fibroblast growth factor receptor expression and disrupts cell mechanics in the developing organ of corti.BMC developmental biology · 2013Article
- The Fibroblast Growth Factor signaling pathway.Wiley interdisciplinary reviews. Developmental biologyReview
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Fibroblast Growth Factor (Fgf) signaling is involved in the exquisite cellular patterning of the developing cochlea, and is necessary for proper hearing function. Our previous data indicate that Fgf signaling disrupts actin, which impacts the surface stiffness of sensory outer hair cells (OHCs) and non-sensory supporting pillar cells (PCs) in the organ of Corti. Here, we used Atomic Force Microscopy (AFM) to measure the impact of loss of function of Fgf-receptor 3, on cytoskeletal formation and cell surface mechanical properties. We find a 50% decrease in both OHC and PC surface stiffness, and a substantial disruption in microtubule formation in PCs. Moreover, we find no change in OHC electromotility of Fgfr3-deficient mice. To further understand the regulation by Fgf-signaling on microtubule formation, we treated wild-type cochlear explants with Fgf-receptor agonist Fgf2, or antagonist SU5402, and find that both treatments lead to a significant reduction in β-Tubulin isotypes I&II. To identify downstream transcriptional targets of Fgf-signaling, we used QPCR arrays to probe 84 cytoskeletal regulators. Of the 5 genes significantly upregulated following treatment, Clasp2, Mapre2 and Mark2 impact microtubule formation. We conclude that microtubule formation is a major downstream effector of Fgf-receptor 3, and suggest this pathway impacts the formation of fluid spaces in the organ of Corti.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.