A transgenic mouse Class‐III β tubulin reporter using yellow fluorescent protein

Liu, Li; Geisert, Eldon E.; Frankfurter, Anthony; Spano, Anthony; Jiang, Chloe Xue; Yue, Junming; Dragatsis, Ioannis; Goldowitz, Dan

doi:10.1002/dvg.20325

Cited by 39 publications

(30 citation statements)

References 32 publications

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“…Each of these three tubulin isotypes are highly expressed in post-mitotic differentiating neurons and the phenotypic similarities suggest they have important overlapping functions (Coksaygan et al, 2006; Jaglin et al, 2009; Liu et al, 2007). However, the primary brain malformations resulting from mutations in TUBA1A and TUBB2B are lissencephaly, pachygyria, and/or grey matter heterotopias that result from cell migration defects.…”

Section: Discussionmentioning

confidence: 99%

Human TUBB3 Mutations Perturb Microtubule Dynamics, Kinesin Interactions, and Axon Guidance

Tischfield

Baris

et al. 2010

Cell

500

556

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We report that eight heterozygous missense mutations in TUBB3, encoding the neuron-specific β-tubulin isotype III, result in a spectrum of human nervous system disorders we now call the TUBB3 syndromes. Each mutation causes the ocular motility disorder CFEOM3, whereas some also result in intellectual and behavioral impairments, facial paralysis, and/or later-onset axonal sensorimotor polyneuropathy. Neuroimaging reveals a spectrum of abnormalities including hypoplasia of oculomotor nerves, and dysgenesis of the corpus callosum, anterior commissure, and corticospinal tracts. A knock-in disease mouse model reveals axon guidance defects without evidence of cortical cell migration abnormalities. We show the disease-associated mutations can impair tubulin heterodimer formation in vitro, although folded mutant heterodimers can still polymerize into microtubules. Modeling each mutation in yeast tubulin demonstrates that all alter dynamic instability whereas a subset disrupts the interaction of microtubules with kinesin motors. These findings demonstrate normal TUBB3 is required for axon guidance and maintenance in mammals.

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Section: Discussionmentioning

confidence: 99%

Human TUBB3 Mutations Perturb Microtubule Dynamics, Kinesin Interactions, and Axon Guidance

Tischfield

Baris

et al. 2010

Cell

500

556

View full text Add to dashboard Cite

show abstract

“…TUBA1A, TUBA8, TUBB2B , and TUBB3 all share similar expression patterns and are the major α and β-tubulin isotypes expressed in the developing brain and nervous system [12, 15, 47, 57]. Considering that microtubules in post-mitotic neurons should contain a mixture of these proteins, differences in the severity and types of brain malformations associated with each tubulin isotype are somewhat surprising.…”

Section: Why Do Mutations In Different Tubulin Isotypes Cause Distincmentioning

confidence: 99%

Distinct α- and β-tubulin isotypes are required for the positioning, differentiation and survival of neurons: new support for the ‘multi-tubulin’ hypothesis

2010

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Synopsis The many functions of the microtubule cytoskeleton are essential for shaping the development and maintaining the operation of the nervous system. With the recent discovery of congenital neurological disorders that result from mutations in genes that encode different α and β-tubulin isotypes (TUBA1A, TUBB2B, TUBA8, and TUBB3), scientists have a novel paradigm to assess how select perturbations in microtubule function affect a range of cellular processes in humans. Moreover, important phenotypic distinctions found among the syndromes suggest that different tubulin isotypes can be utilized for distinct cellular functions during nervous system development. In the present paper, we review: (i) the spectrum of congenital nervous system diseases that result from mutations in tubulin and microtubule associated proteins (MAPs); (ii) the known or putative roles of these proteins during nervous system development; (iii) how the findings collectively support the “multi-tubulin” hypothesis, which postulates that different tubulin isotypes may be required for specialized microtubule functions.

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“…There has been a transgenic mouse Class-III β tubulin reporter which expresses yellow fluorescent protein (YFP) under the control of a 3-kb promoter [14]. This transgenic mouse line could indeed report the Tubb3 expression during neuronal development, but there were some spatial and temporal differences between transgene expression and the endogenous Class III β-tubulin.…”

Section: Discussionmentioning

confidence: 99%

A bacterial artificial chromosome transgenic mouse model for visualization of neurite growth

Tao

Chen

Sun

et al. 2015

Sci. China Life Sci.

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Class III β-tubulin (Tubb3) is a component of the microtubules in neurons and contributes to microtubule dynamics that are required for axon outgrowth and guidance during neuronal development. We here report a novel bacterial artificial chromosome (BAC) transgenic mouse line that expresses Class III β-tubulin fused to mCherry, an improved monomeric red fluorescent protein, for the visualization of microtubules during neuronal development. A BAC containing Tubb3 gene was modified by insertion of mCherry complementary DNA downstream of Tubb3 coding sequence via homologous recombination. mCherry fusion protein was expressed in the nervous system and testis of the transgenic animal, and the fluorescent signal was observed in the neurons that located in the olfactory bulb, cerebral cortex, hippocampal formation, cerebellum, as well as the retina. Besides, Tubb3-mCherry fusion protein mainly distributed in neurites and colocalized with endogenous Class III β-tubulin. The fusion protein labels Purkinje cell dendrites during cerebellar circuit formation. Therefore, this transgenic line might be a novel tool for scientific community to study neuronal development both in vitro and in vivo.

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A transgenic mouse Class‐III β tubulin reporter using yellow fluorescent protein

Cited by 39 publications

References 32 publications

Human TUBB3 Mutations Perturb Microtubule Dynamics, Kinesin Interactions, and Axon Guidance

Human TUBB3 Mutations Perturb Microtubule Dynamics, Kinesin Interactions, and Axon Guidance

Distinct α- and β-tubulin isotypes are required for the positioning, differentiation and survival of neurons: new support for the ‘multi-tubulin’ hypothesis

A bacterial artificial chromosome transgenic mouse model for visualization of neurite growth

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