ArticlePLoS genetics2019
Differential requirements of tubulin genes in mammalian forebrain development.
Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 63 citations in OpenAlex.
- Differential contributions of β-tubulin isotypes to acentrosomal oocyte meiosis in C. elegans.The Journal of cell biology · 2026Article
- Spatial transcriptomics reveal developmental dynamics of the human cerebral cortex and striatum.Science China. Life sciences · 2026Article
- Restoring the Balance: CRISPRa-Driven β-Tubulin Compensation as a Strategy for Tubulinopathy Treatment.International journal of molecular sciences · 2026Article
- Bridging the gap: an emerging link between tubulinopathies and ciliopathies.NPJ genomic medicine · 2026Review
- TUBB2A related epilepsy: novel variants and genotype-phenotype correlation.Scientific reports · 2026Article
- Ttc21b is required for proper proliferation of neural progenitor cells.Disease models & mechanisms · 2026Article
- Differential contributions of β-tubulin isotypes to acentrosomal oocyte meiosis inbioRxiv : the preprint server for biology · 2025Article
- RNF187 Facilitates Proliferation and Migration of Human Spermatogonial Stem Cells Through WDR77 Polyubiquitination.Cell proliferation · 2025Article
- Learning-efficient spiking neural networks with multi-compartment spatio-temporal backpropagation.iScience · 2025Article
- Synergism between TLR4 and B. infantis in the development of the premature intestine.Pediatric research · 2025Article
- Identification of markers for neurescence through transcriptomic profiling of postmortem human brains.npj aging · 2025Article
- Identification of markers for neurescence through transcriptomic profiling of postmortem human brains.Research square · 2025Article
- Developmental and Epileptic Encephalopathy: Pathogenesis of Intellectual Disability Beyond Channelopathies.Biomolecules · 2025Review
- SMPD4-mediated sphingolipid metabolism regulates brain and primary cilia development.Development (Cambridge, England) · 2024Article
- Deciphering the role of sphingolipid metabolism in the immune microenvironment and prognosis of esophageal cancer via single-cell sequencing and bulk data analysis.Discover oncology · 2024Article
- TUBB4B is essential for the cytoskeletal architecture of cochlear supporting cells and motile cilia development.Communications biology · 2024Article
- Tubb4b is required for multi-ciliogenesis in the mouse.Development (Cambridge, England) · 2024Article
- Insights on the Role of α- and β-Tubulin Isotypes in Early Brain Development.Molecular neurobiology · 2023Review
- Proteomics and cytokine analyses distinguish myalgic encephalomyelitis/chronic fatigue syndrome cases from controls.Journal of translational medicine · 2023Article
- CRISPR/Cas9 andInternational journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Tubulin genes encode a series of homologous proteins used to construct microtubules which are essential for multiple cellular processes. Neural development is particularly reliant on functional microtubule structures. Tubulin genes comprise a large family of genes with very high sequence similarity between multiple family members. Human genetics has demonstrated that a large spectrum of cortical malformations are associated with de novo heterozygous mutations in tubulin genes. However, the absolute requirement for many of these genes in development and disease has not been previously tested in genetic loss of function models. Here we directly test the requirement for Tuba1a, Tubb2a and Tubb2b in the mouse by deleting each gene individually using CRISPR-Cas9 genome editing. We show that loss of Tubb2a or Tubb2b does not impair survival but does lead to relatively mild cortical malformation phenotypes. In contrast, loss of Tuba1a is perinatal lethal and leads to significant forebrain dysmorphology. We also present a novel mouse ENU allele of Tuba1a with phenotypes similar to the null allele. This demonstrates the requirements for each of the tubulin genes and levels of functional redundancy are quite different throughout the gene family. The ability of the mouse to survive in the absence of some tubulin genes known to cause disease in humans suggests future intervention strategies for these devastating tubulinopathy diseases.
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Registered trials
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.