Ideal type 1 is caused by a point mutation in the a-tubulin gene that affects microtubule arrangement in soybean

Plant architecture is a target of crop improvement.The soybean mutant ideal type 1(it1)displays a pleiotropic phenotype characterized by compact plant architecture,reduced plant height,shortened petioles,wrinkled leaves,and indented seeds.Genetic analysis revealed that the pleiotropic phenotype was controlled by an incomplete dominant gene.We characterized the cellular phenotypes of it1 and positionally cloned the it1 locus.Detailed morphogenetic analysis of the it1 mutant revealed an excess of xylem cells and expanded phloem,and polygonal pavement cells.Positional cloning showed that the phenotype was caused by a G-to-A mutation in the second exon of the a-tubulin gene(Glyma.05G157300).The mutation altered microtubule arrangement in pavement cells,changing their morphology.Overexpression of Gmit1 resulted in an it1-like phenotype and polygonal pavement cells and microtubules of overexpressors were parallel or slightly inclined.Five suppressor mutants able to suppress the phenotype of it1 were obtained by EMS mutagenesis in the it1 background.All these mutants carried an additional mutation in the it1 gene.These results suggest that the pleiotropic phenotype of it1 is caused by the mutation in the atubulin gene.

Alpha-tubulin deacetylase as a potential and novel target for the prevention of Parkinson's disease progression

Parkinson＇s disease （PD） is the second most common neurodegenerative disorder and is characterized by its progressive course. The current therapies are aimed at alleviating symptoms by rescuing the unbalanced physiological dopamine metabolism and recovery of damaged neuronal circuits. However, these strategies result in insufficient clinical benefits for many patients and fail to halt disease progression. Therefore, new therapeutic targets could serve as the gateway against PD degeneration. One pathological hallmark of PD is the formation of intracytoplasmic protein inclusions or Lewy bodies, in neurons. Recent studies have suggested that Lewy bodies are formed similarly to aggresomes, and results have supported the concept that the novel cellular organelle, the aggresome, is a cytoprotective response that sequesters and facilitates clearance of potentially toxic protein aggregates. In addition, a-tubulin deacetylase has been shown to regulate aggresome formation and rescue neural cell viability in response to misfolded protein. Therefore, the regulation of aggresome formation to trigger cellular self-protection system could arrest PD progression. The present study discusses research progress related to Lewy bodies, aggresomes, and histone deacetylases, with an emphasis on histone deacetylase 6 and sirtuin type 2.

Evidence for a mouse brain-specific variant of α-tubulin

While studying the neural precursor cell intermediatefilament protein known as nestin in the developing mousebrain, we observed a strong cross-reaction of our nestin antibody with a 50 kDa protein that appeared on embryonicday 10 and continued to accumulate until postnatal day 1.Here we report evidence that this protein is a brain-specificvariant form of or-tubulin and discuss its implications.