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FUNCTIONS OF MSX2 AND MSX1 DURING MOUSE SKULL AND HAIR FOLLICLE DEVELOPMENT by Hualin Fu ____________________________________________________________ A Dissertation Presented to the FACULTY OF THE GRADUATE SCHOOL UNIVERSITY OF SOUTHERN CALIFORNIA In Partial Fulfillment of the Requirements for the Degree DOCTOR OF PHILOSOPHY (BIOCHEMISTRY AND MOLECULAR BIOLOGY) May 2007 Copyright 2007 Hualin Fu
Object Description
Title | Functions of Msx2 and Msx1 during mouse skull and hair follicle development |
Author | Fu, Hualin |
Author email | hfu@usc.edu |
Degree | Doctor of Philosophy |
Document type | Dissertation |
Degree program | Biochemistry & Molecular Biology |
School | Keck School of Medicine |
Date defended/completed | 2006-12-07 |
Date submitted | 2007 |
Restricted until | Restricted until 14 Feb. 2009. |
Date published | 2009-02-14 |
Advisor (committee member) |
Maxson, Robert E. Laird, Peter W. Roy-Burman, Pradip |
Abstract | Conditional targeting was used to identify the tissues in which Msx2 functions during calvarial development. Epidermis inactivation of Msx2 does not produce skull defects. Inactivation of Msx2 in the calvarial osteogenic mesenchyme resulted in a defect comparable to that of germline knockouts. Inactivation of Msx2 in neural crest-derived mesenchyme and Dura resulted in a smaller frontal bone defect and no parietal bone defect. Mesoderm inactivation of Msx2 did not induce a frontal foramen but did shorten the parietal bone. These results suggest (i) that Msx2 functions in the osteogenic mesenchyme from both mesoderm and neural crest origin, and (ii) that Msx2 is not required in the Dura for parietal bone development. Moreover, the position of the coronal suture shifted more posterior in the mesoderm knockout but more towards the frontal bone in the neural crest knockout, suggesting that the skull patterning was affected by changing Msx2 activity. Furthermore, massive cell proliferation and a constitutive alkaline phosphatase activity were observed in the osteogenic mesenchyme throughout different stages of skull development. Genetic labeling tracing indicated that the cells in both coronal and sagittal suture mesenchyme give rise to new bones at the flanking bone fronts. The tissue layer structure of suture mesenchyme seemed to be changing overtime as measured by collagen type I immunostaining. A collagen type I degradation enzyme MT1 was expressed at lower level at osteogenic fronts in Msx2 mutant than in controls. Msx2 might regulate the ECM remodeling process during the skull development.; Msx2 mutant mice also have defects in hair follicle development and cycling. Inactivation of Msx2 in skin epidermis resulted in hair defects resembling the Msx2 conventional mutant. Inactivation of Msx2 in hair follicle dermal papilla and the dermis did not induce the hair defect. Neither mutation of Msx1 in the dermis nor in the epidermis causes a hair defect. These results suggest (i) that Msx2 functions autonomously in the skin epithelium to regulate hair follicle development (ii) that Msx1 is not required for hair development. |
Keyword | Msx2; Msx1; skull; hair follicle; knockout mice; Cre/Lox |
Language | English |
Part of collection | University of Southern California dissertations and theses |
Publisher (of the original version) | University of Southern California |
Place of publication (of the original version) | Los Angeles, California |
Publisher (of the digital version) | University of Southern California. Libraries |
Type | texts |
Legacy record ID | usctheses-m256 |
Contributing entity | University of Southern California |
Rights | Fu, Hualin |
Repository name | Libraries, University of Southern California |
Repository address | Los Angeles, California |
Repository email | cisadmin@lib.usc.edu |
Filename | etd-Fu-20070214 |
Archival file | uscthesesreloadpub_Volume29/etd-Fu-20070214.pdf |
Description
Title | Page 1 |
Contributing entity | University of Southern California |
Repository email | cisadmin@lib.usc.edu |
Full text | FUNCTIONS OF MSX2 AND MSX1 DURING MOUSE SKULL AND HAIR FOLLICLE DEVELOPMENT by Hualin Fu ____________________________________________________________ A Dissertation Presented to the FACULTY OF THE GRADUATE SCHOOL UNIVERSITY OF SOUTHERN CALIFORNIA In Partial Fulfillment of the Requirements for the Degree DOCTOR OF PHILOSOPHY (BIOCHEMISTRY AND MOLECULAR BIOLOGY) May 2007 Copyright 2007 Hualin Fu |