ArticleThe Journal of biological chemistry
Nonredundant roles of DIAPHs in primary ciliogenesis.
Article in The Journal of biological chemistry. 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, 9 citations in OpenAlex.
- The Role of Microfilaments in Cilia Formation and Function.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Piezo1, F-Actin Remodeling, and Podocyte Survival and Regeneration.Journal of the American Society of Nephrology : JASN · 2025Article
- Actin cytoskeletal regulation of ciliogenesis in development and disease.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- mDia formins form hetero-oligomers and cooperatively maintain murine hematopoiesis.PLoS genetics · 2023Article
- Primary cilia and actin regulatory pathways in renal ciliopathies.Frontiers in nephrology · 2023Review
- Review
- Diaph3 underlines tumor cell heterogeneity in glioblastoma with implications for treatment modalities resistance.Journal of neuro-oncology · 2022Article
- Metabolic Regulation of Inflammation and Its Resolution: Current Status, Clinical Needs, Challenges, and Opportunities.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Diaphanous related formin 3 knockdown suppresses cell proliferation and metastasis of osteosarcoma cells.Discover oncology · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary cilia are hubs for several signaling pathways, and disruption in cilia function and formation leads to a range of diseases collectively known as ciliopathies. Both ciliogenesis and cilia maintenance depend on vesicle trafficking along a network of microtubules and actin filaments toward the basal body. The DIAPH (Diaphanous-related) family of formins promote both actin polymerization and microtubule (MT) stability. Recently, we showed that the formin DIAPH1 is involved in ciliogenesis. However, the role of other DIAPH family members in ciliogenesis had not been investigated. Here we show that depletion of either DIAPH2 or DIAPH3 also disrupted ciliogenesis and cilia length. DIAPH3 depletion also reduced trafficking within cilia. To specifically examine the role of DIAPH3 at the base, we used fused full-length DIAPH3 to centrin, which targeted DIAPH3 to the basal body, causing increased trafficking to the ciliary base, an increase in cilia length, and formation of bulbs at the tips of cilia. Additionally, we confirmed that the microtubule-stabilizing properties of DIAPH3 are important for its cilia length functions and trafficking. These results indicate the importance of DIAPH proteins in regulating cilia maintenance. Moreover, defects in ciliogenesis caused by DIAPH depletion could only be rescued by expression of the specific family member depleted, indicating nonredundant roles for these proteins.
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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.