Embryonic Stem Cells and Transgenic Mice Ubiquitously Expressing a Tau-Tagged Green Fluorescent Protein

Pratt, Thomas; Sharp, Linda; Nichols, Jennifer; Price, David J.; Mason, John O.

doi:10.1006/dbio.2000.9935

Cited by 112 publications

(114 citation statements)

References 32 publications

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“…B6 mice (The Jackson Laboratory, Bar Harbor, ME) were used for most experiments. In addition, reeler mice (B6C3Fe a/a-Reln rl /J; The Jackson Laboratory), tau-GFP transgenic mice (Pratt et al, 2000), and Math1 mutant mice (Math1 lacZ and Math1 Ϫ ) (Wang et al, 2005) were used for some experiments where indicated. The mice were used according to a protocol approved by the Institutional Animal Care and Use Committee at the University of Washington.…”

Section: Methodsmentioning

confidence: 99%

Unipolar Brush Cells of the Cerebellum Are Produced in the Rhombic Lip and Migrate through Developing White Matter

Englund¹,

Kowalczyk²,

Daza³

et al. 2006

J. Neurosci.

223

253

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Section: Methodsmentioning

confidence: 99%

Unipolar Brush Cells of the Cerebellum Are Produced in the Rhombic Lip and Migrate through Developing White Matter

Englund¹,

Kowalczyk²,

Daza³

et al. 2006

J. Neurosci.

223

253

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“…For each marker and each stage, three to five nonexencephalic embryos were analyzed at rostral, medial, and caudal levels of the developing forebrain. Golli-GFP (Jacobs et al, 2007) and GFP mice (Pratt et al, 2000) were bred into the Pdn line.…”

Section: Methodsmentioning

confidence: 99%

TheGli3Hypomorphic MutationPdnCauses Selective Impairment in the Growth, Patterning, and Axon Guidance Capability of the Lateral Ganglionic Eminence

Magnani¹,

Hasenpusch‐Theil²,

Jacobs³

et al. 2010

J. Neurosci.

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Previous studies have defined a requirement for Sonic hedgehog (Shh) signaling in patterning the ventral telencephalon, a major source of the neuronal diversity found in the mature telencephalon. The zinc finger transcription factor Gli3 is a critical component of the Shh signaling pathway and its loss causes major defects in telencephalic development. Gli3 is expressed in a graded manner along the dorsoventral axis of the telencephalon but it is unknown whether Gli3 expression levels are important for dorsoventral telencephalic patterning. To address this, we used the Gli3 hypomorphic mouse mutant Polydactyly Nagoya (Pdn). We show that in Pdn/Pdn embryos, the telencephalic expression of Gli3 remains graded, but Gli3 mRNA and protein levels are reduced, resulting in an upregulation of Shh expression and signaling. These changes mainly affect the development of the lateral ganglionic eminence (LGE), with some disorganization of the medial ganglionic eminence mantle zone. The pallial/subpallial boundary is shifted dorsally and the production of postmitotic neurons is reduced. Moreover, LGE pioneer neurons that guide corticofugal axons into the LGE do not form properly, delaying the entry of corticofugal axons into the ventral telencephalon. Pdn/Pdn mutants also show severe pathfinding defects of thalamocortical axons in the ventral telencephalon. Transplantation experiments demonstrate that the intrinsic ability of the Pdn ventral telencephalon to guide thalamocortical axons is compromised. We conclude that correct Gli3 levels are particularly important for the LGE's growth, patterning, and development of axon guidance capabilities.

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“…p16 and pl6 P114L were cloned as XhoI fragments into pCAGiP (Pratt et al, 2000), such that their expression was under the control of the CAG promoter. A measure of 10-20 mg of ScaI-linearized pCAG.p16 and pCAG.p16 Pll4L DNA was electroporated into ES cells (3-5 Â 10 7 cells) using a BioRad Gene Pulser (200 V, 500 mF).…”

Section: Stable Expression Of P16 Ink4a In Es Cellsmentioning

confidence: 99%

Cdk6–cyclin D3 activity in murine ES cells is resistant to inhibition by p16INK4a

et al. 2004

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Through a screen aimed at identifying genes that are specifically upregulated in embryomic stem (ES) cells but not primitive ectoderm, we identified cyclin D3. This was surprising since cyclin D activity is generally believed to be inactive in ES cells even though retinoblastoma tumor suppressor protein (pRb) accumulates in a predominantly hyperphosphorylated state. Cdk6 is the major catalytic partner for cyclin D3 in ES cells and exhibits robust pRb kinase activity that is downregulated during the early stages of ES embryoid body differentiation. To investigate the basis underlying the insensitivity of ES cells to ectopic p16 expression, we show that Cdk6-cyclin D3 complexes are not subject to inhibition by p16, similar to Cdk-viral cyclin complexes. These observations show that specificity exists between Cdk4/6-cyclin D complexes and their ability to be targeted by p16. Our data suggest that Cdk6-cyclin D3 activity in other cell types, including tumors, may also be refractory to p16-mediated growth inhibition and raises the possibility of additional specificity within the INK4 family.

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Embryonic Stem Cells and Transgenic Mice Ubiquitously Expressing a Tau-Tagged Green Fluorescent Protein

Cited by 112 publications

References 32 publications

Unipolar Brush Cells of the Cerebellum Are Produced in the Rhombic Lip and Migrate through Developing White Matter

Unipolar Brush Cells of the Cerebellum Are Produced in the Rhombic Lip and Migrate through Developing White Matter

TheGli3Hypomorphic MutationPdnCauses Selective Impairment in the Growth, Patterning, and Axon Guidance Capability of the Lateral Ganglionic Eminence

Cdk6–cyclin D3 activity in murine ES cells is resistant to inhibition by p16INK4a

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