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The repressor form of Gli3 plays a c...

Meyer, Neva P.

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The repressor form of Gli3 plays a critical role in dorsoventral fate specification in the developing spinal cord.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The repressor form of Gli3 plays a critical role in dorsoventral fate specification in the developing spinal cord./
Author:	Meyer, Neva P.
Description:	97 p.
Notes:	Chair: Henk Roelink.
Contained By:	Dissertation Abstracts International66-12B.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3198822
ISBN:	9780542443671

The repressor form of Gli3 plays a critical role in dorsoventral fate specification in the developing spinal cord.
Meyer, Neva P.

The repressor form of Gli3 plays a critical role in dorsoventral fate specification in the developing spinal cord. - 97 p.

Chair: Henk Roelink.

Thesis (Ph.D.)--University of Washington, 2005.

During development, the vertebrate CNS is patterned along the dorsoventral axis to give rise to motor neurons, interneurons and sensory neurons. In the ventral neural tube, Shh initiates expression of ventral, class II progenitor proteins while repressing expression of dorsal, class I progenitor proteins. The mutual repression between pairs of class I and class II progenitors serves to sharpen abutting boundaries thus creating discrete domains of overlapping progenitor protein expression from which specific types of neurons differentiate. Loss of Shh results in a loss of stereotypical domains of progenitor protein expression and almost all ventral cell types in the spinal cord. The zinc finger-containing transcription factors Gli1, 2 and 3 mediate the Shh response. Part of the shh-/- phenotype is compensated in the absence of Gli3, consistent with the predicted role of Gli3 as a repressor of the Shh response. The cleavage of Gli3, which generates a transcriptional repressor, is blocked by Shh, stabilizing an activator form of Gli3. In order to test the role of the repressor form of Gli3 in the neural tube, a truncated version of Gli3 (Gli3R*) lacking the activation domain was created. Gli3R* acts as a constitutive repressor of the Shh response. Misexpression of Gli3R* in the chick neural tube caused a ventral expansion of class I, dorsal progenitor proteins and a loss of class II, ventral progenitor proteins. The expansion of class I proteins upon Gli3R* misexpression appears to be mediated by repression of class II protein expression and the concomitant loss of class I protein inhibition. In the dorsal neural tube, a gradient of BMP activity can pattern progenitor protein expression and antagonize the Shh response. In neural plate explants increasing amounts of BMP4 are able to dorsalize Shh-ventralized tissue and, at least in naive tissue, to maintain gli3 expression, which may be one mechanism of antagonism of the Shh reponse. Thus, dorsoventral fate specification in the neural tube can be controlled by multiple signals, demonstrating the robust nature of CNS patterning.

ISBN: 9780542443671Subjects--Topical Terms:

1017719
Biology, Molecular.

The repressor form of Gli3 plays a critical role in dorsoventral fate specification in the developing spinal cord.
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100 1 $a Meyer, Neva P. $3 1267671
245 1 4 $a The repressor form of Gli3 plays a critical role in dorsoventral fate specification in the developing spinal cord.
300 $a 97 p.
500 $a Chair: Henk Roelink.
500 $a Source: Dissertation Abstracts International, Volume: 66-12, Section: B, page: 6458.
502 $a Thesis (Ph.D.)--University of Washington, 2005.
520 $a During development, the vertebrate CNS is patterned along the dorsoventral axis to give rise to motor neurons, interneurons and sensory neurons. In the ventral neural tube, Shh initiates expression of ventral, class II progenitor proteins while repressing expression of dorsal, class I progenitor proteins. The mutual repression between pairs of class I and class II progenitors serves to sharpen abutting boundaries thus creating discrete domains of overlapping progenitor protein expression from which specific types of neurons differentiate. Loss of Shh results in a loss of stereotypical domains of progenitor protein expression and almost all ventral cell types in the spinal cord. The zinc finger-containing transcription factors Gli1, 2 and 3 mediate the Shh response. Part of the shh-/- phenotype is compensated in the absence of Gli3, consistent with the predicted role of Gli3 as a repressor of the Shh response. The cleavage of Gli3, which generates a transcriptional repressor, is blocked by Shh, stabilizing an activator form of Gli3. In order to test the role of the repressor form of Gli3 in the neural tube, a truncated version of Gli3 (Gli3R*) lacking the activation domain was created. Gli3R* acts as a constitutive repressor of the Shh response. Misexpression of Gli3R* in the chick neural tube caused a ventral expansion of class I, dorsal progenitor proteins and a loss of class II, ventral progenitor proteins. The expansion of class I proteins upon Gli3R* misexpression appears to be mediated by repression of class II protein expression and the concomitant loss of class I protein inhibition. In the dorsal neural tube, a gradient of BMP activity can pattern progenitor protein expression and antagonize the Shh response. In neural plate explants increasing amounts of BMP4 are able to dorsalize Shh-ventralized tissue and, at least in naive tissue, to maintain gli3 expression, which may be one mechanism of antagonism of the Shh reponse. Thus, dorsoventral fate specification in the neural tube can be controlled by multiple signals, demonstrating the robust nature of CNS patterning.
590 $a School code: 0250.
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791 $a Ph.D.
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