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The role of the TALE homeodomain pro...

Rhee, Joon Whan.

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The role of the TALE homeodomain protein Pbx3 in murine development and respiration.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	The role of the TALE homeodomain protein Pbx3 in murine development and respiration./
Author:	Rhee, Joon Whan.
Description:	91 p.
Notes:	Adviser: Michael L. Cleary.
Contained By:	Dissertation Abstracts International63-04B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3048602
ISBN:	0493629998

The role of the TALE homeodomain protein Pbx3 in murine development and respiration.
Rhee, Joon Whan.

The role of the TALE homeodomain protein Pbx3 in murine development and respiration. - 91 p.

Adviser: Michael L. Cleary.

Thesis (Ph.D.)--Stanford University, 2002.

TALE (three amino acid loop extension) homeodomain proteins are critical regulators of developmental gene expression which form transcriptionally active DNA binding complexes. To study the developmental role of this TALE protein, Pbx3 null mutant mice were constructed using gene targeting techniques. Pbx3 deficient mice developed to term with no apparent anatomic abnormalities but quickly expired due to apparent respiratory difficulties. Whole body plethysmography showed that Pbx3 −/− neonates had both a lower frequency and amplitude of respiration versus their viable littermates. These observations are consistent with the hypothesis that hypoventilation is the likely cause of death of Pbx3 null neonates. C4 ventral root activity was recorded in medullaspinal cord preparations to further localize the respiratory defect and was consistent with the plethysmography readings. To determine if the altered respiratory pattern was due to defects in the inspiratory neurons of the ventral medulla, membrane potentials were assessed. The latter correlated with the C4 recordings indicating that the respiratory defect seen in Pbx3 deficient neonates results from a dysfunction of the central respiratory network in the ventral medulla. Mice deficient for the meta-Hox gene Rnx (Hox11L2) display an apparent central respiratory defect. Co-immunofluorescence experiments revealed that both Pbx3 and Rnx are present in the same cells in the ventral portion of the medulla oblongata thought to be an important respiratory control center. Electrophoretic mobility shift assays (EMSA's) were performed using a modified HoxB2 RARE DNA element and showed that in conjunction with another transcription factor, Meis1, Pbx3 and Rnx formed stable trimeric DNA binding complexes. Transient transfection assays confirmed the transcriptional ability of this trimeric complex. Taken together, the observed respiratory phenocopy of Pbx3 and Rnx deficient mice, the co-expression of Pbx3 and Rnx in a critical respiratory center in the brainstem, and their ability to form stable and transcriptionally active complexes on relevant DNA regulatory elements, all suggest that Pbx3 and Rnx may form functional DNA binding complexes that initiate expression of target genes essential for the normal development of inspiratory neuronal network in the ventrolateral medulla.

ISBN: 0493629998Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The role of the TALE homeodomain protein Pbx3 in murine development and respiration.
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035 $a (UnM)AAI3048602
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100 1 $a Rhee, Joon Whan. $3 1251310
245 1 0 $a The role of the TALE homeodomain protein Pbx3 in murine development and respiration.
300 $a 91 p.
500 $a Adviser: Michael L. Cleary.
500 $a Source: Dissertation Abstracts International, Volume: 63-04, Section: B, page: 1709.
502 $a Thesis (Ph.D.)--Stanford University, 2002.
520 $a TALE (three amino acid loop extension) homeodomain proteins are critical regulators of developmental gene expression which form transcriptionally active DNA binding complexes. To study the developmental role of this TALE protein, Pbx3 null mutant mice were constructed using gene targeting techniques. Pbx3 deficient mice developed to term with no apparent anatomic abnormalities but quickly expired due to apparent respiratory difficulties. Whole body plethysmography showed that Pbx3 −/− neonates had both a lower frequency and amplitude of respiration versus their viable littermates. These observations are consistent with the hypothesis that hypoventilation is the likely cause of death of Pbx3 null neonates. C4 ventral root activity was recorded in medullaspinal cord preparations to further localize the respiratory defect and was consistent with the plethysmography readings. To determine if the altered respiratory pattern was due to defects in the inspiratory neurons of the ventral medulla, membrane potentials were assessed. The latter correlated with the C4 recordings indicating that the respiratory defect seen in Pbx3 deficient neonates results from a dysfunction of the central respiratory network in the ventral medulla. Mice deficient for the meta-Hox gene Rnx (Hox11L2) display an apparent central respiratory defect. Co-immunofluorescence experiments revealed that both Pbx3 and Rnx are present in the same cells in the ventral portion of the medulla oblongata thought to be an important respiratory control center. Electrophoretic mobility shift assays (EMSA's) were performed using a modified HoxB2 RARE DNA element and showed that in conjunction with another transcription factor, Meis1, Pbx3 and Rnx formed stable trimeric DNA binding complexes. Transient transfection assays confirmed the transcriptional ability of this trimeric complex. Taken together, the observed respiratory phenocopy of Pbx3 and Rnx deficient mice, the co-expression of Pbx3 and Rnx in a critical respiratory center in the brainstem, and their ability to form stable and transcriptionally active complexes on relevant DNA regulatory elements, all suggest that Pbx3 and Rnx may form functional DNA binding complexes that initiate expression of target genes essential for the normal development of inspiratory neuronal network in the ventrolateral medulla.
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