東華大學圖書館 |

Language: English

Help

回圖書館首頁

手機版館藏查詢

Back

Switch To: Labeled | MARC Mode | ISBD

Tubby-like Protein 3 (Tulp3) regulat...

Norman, Ryan Andrew.

Linked to FindBook

Google Book

Amazon

博客來

Tubby-like Protein 3 (Tulp3) regulates patterning in the mouse embryo through inhibition of sonic hedgehog signaling.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Tubby-like Protein 3 (Tulp3) regulates patterning in the mouse embryo through inhibition of sonic hedgehog signaling./
Author:	Norman, Ryan Andrew.
Description:	135 p.
Notes:	Source: Dissertation Abstracts International, Volume: 71-06, Section: B, page: 3448.
Contained By:	Dissertation Abstracts International71-06B.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3410914
ISBN:	9781124047713

Tubby-like Protein 3 (Tulp3) regulates patterning in the mouse embryo through inhibition of sonic hedgehog signaling.
Norman, Ryan Andrew.

Tubby-like Protein 3 (Tulp3) regulates patterning in the mouse embryo through inhibition of sonic hedgehog signaling. - 135 p.

Source: Dissertation Abstracts International, Volume: 71-06, Section: B, page: 3448.

Thesis (Ph.D.)--Princeton University, 2010.

Neural patterning within the mammalian spinal cord and brain relies upon signaling cues from surrounding tissues, and the mouse neural tube serves as a good model to uncover genes involved in neural patterning. Through analysis of recessive mutations causing developmental and neural tube dorso-ventral patterning defects, novel Sonic hedgehog (Shh) signaling components can be identified and characterized based on changes in Shh-dependent cell identities. This work characterizes Tubby-like Protein 3 (Tulp3 ) as a novel negative regulator of Shh signaling in the mouse embryo. Tulp3 is required for proper embryonic development in mice; genetic disruption of mouse Tulp3 generates morphological defects in the embryonic craniofacial regions, spinal cord, and limbs. In Tulp3 mutants, ventral cell types in the neural tube are ectopically specified at the expense of dorsal cell types. These ventral cell types acquire their identity primarily from Shh signaling, suggesting that Tulp3 mutants de-repress Shh signaling.

ISBN: 9781124047713Subjects--Topical Terms:

1017719
Biology, Molecular.

Tubby-like Protein 3 (Tulp3) regulates patterning in the mouse embryo through inhibition of sonic hedgehog signaling.
LDR:03439nam 2200301 4500 001 1402996
005 20111108080344.5
008 130515s2010 ||||||||||||||||| ||eng d
020 $a 9781124047713
035 $a (UMI)AAI3410914
035 $a AAI3410914
040 $a UMI $c UMI
100 1 $a Norman, Ryan Andrew. $3 1682227
245 1 0 $a Tubby-like Protein 3 (Tulp3) regulates patterning in the mouse embryo through inhibition of sonic hedgehog signaling.
300 $a 135 p.
500 $a Source: Dissertation Abstracts International, Volume: 71-06, Section: B, page: 3448.
500 $a Adviser: Jonathan T. Eggenschwiler.
502 $a Thesis (Ph.D.)--Princeton University, 2010.
520 $a Neural patterning within the mammalian spinal cord and brain relies upon signaling cues from surrounding tissues, and the mouse neural tube serves as a good model to uncover genes involved in neural patterning. Through analysis of recessive mutations causing developmental and neural tube dorso-ventral patterning defects, novel Sonic hedgehog (Shh) signaling components can be identified and characterized based on changes in Shh-dependent cell identities. This work characterizes Tubby-like Protein 3 (Tulp3 ) as a novel negative regulator of Shh signaling in the mouse embryo. Tulp3 is required for proper embryonic development in mice; genetic disruption of mouse Tulp3 generates morphological defects in the embryonic craniofacial regions, spinal cord, and limbs. In Tulp3 mutants, ventral cell types in the neural tube are ectopically specified at the expense of dorsal cell types. These ventral cell types acquire their identity primarily from Shh signaling, suggesting that Tulp3 mutants de-repress Shh signaling.
520 $a From genetic epistasis experiments, we show that the Tulp3 ventralized phenotype occurs independently of Shh, the transmembrane protein Smoothened, and transcription factor Gli3. Tulp3 is, however, dependent upon the transcription factor Gli2 and kinesin II subunit Kif3A, which regulates intraflagellar transport and formation of the primary cilium. Tulp3 also localizes to the cilium, a site where other Shh components Smoothened, Gli transcription factors, and Suppressor of Fused are found. Although trafficking or processing events occurring in the cilium are not well understood, biochemical data from other organisms suggest that members of the Tubby family of proteins function in vesicular trafficking and/or signaling mediated through the cilium. Importantly, Tulp3 mutants do assemble primary cilia of normal length, but demonstrate loss of another Shh regulator Arl13b in neural tube cilia, indicating that Tulp3 may regulate trafficking of Arl13b. Further genetic epistasis suggests that in addition to Arl13b, Tulp3 may regulate other unknown components for ventral neural patterning. This work lastly identifies a Tulp3 protein interaction with CaMKII, a kinase involved in Ca2+-dependent responses, as one of these potential components. Through these genetic and biochemical analyses of Tulp3 function, we have gained further insight to the complexities and regulation unique to mammalian Shh signal transduction.
590 $a School code: 0181.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Biology, Genetics. $3 1017730
690 $a 0307
690 $a 0317
690 $a 0369
710 2 $a Princeton University. $3 645579
773 0 $t Dissertation Abstracts International $g 71-06B.
790 1 0 $a Eggenschwiler, Jonathan T., $e advisor
790 $a 0181
791 $a Ph.D.
792 $a 2010
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3410914