Poster abstracts
Poster number 29 submitted by Ramon Macias
Beta tubulins in the developing brain compensate for the loss of Tubb2a and Tubb2b
Ramon Macias (Molecular, Cellular, and Developmental Biology Graduate Program), Rolf W. Stottmann (Pediatrics, Ohio State University and Nationwide Childrens Hospital)
Abstract:
Beta tubulin genes are critical elements of the cytoskeleton, yet their individual expression patterns and functional contributions in development are under-studied. Using novel epitope-tagged knock-in mouse models, we characterized TUBB2A and TUBB2B protein expression at tissue, cellular, and organelle resolution across embryonic and postnatal development. Both proteins are strongly expressed in differentiated neurons and minimally expressed in neural progenitors. Neither protein is present at detectable levels in primary or motile cilia. Building on these expression patterns, genetic experiments revealed that removing both Tubb2a and Tubb2b, whether specifically in the forebrain or across the entire embryo, didn’t disrupt overall brain structure. Interestingly, when both genes were deleted, transcriptomic analysis revealed increased expression of other tubulin genes, suggesting that the brain can compensate for the loss of Tubb2a and Tubb2b by adjusting the expression of related genes. These findings indicate that beta tubulin genes have a high degree of functional redundancy in the brain. This insight may open new therapeutic possibilities for patients with dominant-negative or gain-of-function variants.
Keywords: Beta Tubulin, Brain Development, Cilia