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Regulation of Mouse Retinal Ganglion...

Jiang, Ying.

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Regulation of Mouse Retinal Ganglion Cell Development by Sox4 and Sox11.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Regulation of Mouse Retinal Ganglion Cell Development by Sox4 and Sox11./
作者:	Jiang, Ying.
面頁冊數:	113 p.
附註:	Source: Dissertation Abstracts International, Volume: 75-02(E), Section: B.
Contained By:	Dissertation Abstracts International75-02B(E).
標題:	Biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3600401
ISBN:	9781303504983

Regulation of Mouse Retinal Ganglion Cell Development by Sox4 and Sox11.
Jiang, Ying.

Regulation of Mouse Retinal Ganglion Cell Development by Sox4 and Sox11. - 113 p.

Source: Dissertation Abstracts International, Volume: 75-02(E), Section: B.

Thesis (Ph.D.)--University of Rochester, 2013.

This item must not be sold to any third party vendors.

The proper functioning of the retina is contingent upon the correct generation of the major cell types. Elucidation of developmental processes that give rise to anatomically and functionally distinct populations is essential for us to understand the proper function of the retina. This work is aimed to identify and functionally characterize novel transcription regulators involved in the development of retinal ganglion cells (RGCs). RGCs are the only projection neurons in the retina. Loss of RGCs results in various retinal diseases, such as glaucoma and other optic neuropathies. However, the genetic program controlling RGC development is largely unknown. Here we show that wide expression of the SoxC genes, Sox4 and Sox11, was observed throughout retinogenesis, particularly with high levels in the ganglion cell layer in an overlapping manner. To test the function of Sox4 and Sox11 in the development of mouse RGCs, we generated Sox4, Sox11 and Sox4/Sox11 conditional knockout (CKO) mice. Although targeted disruption of either Sox4 or Sox11 in retinas led to a mild reduction in the number of RGCs, combined deletion of Sox4 and Sox11 in the retina resulted in an abolishment of RGCs. Our developmental analysis demonstrates that Sox4 and Sox11 function redundantly to regulate the generation of RGCs at early embryonic stages as well as the survival of RGCs at late embryonic stages. Furthermore, genetic analysis reveals that Sox4 and Sox11 function between Math5 and Brn3b in the RGC regulatory pathway. In addition, overexpression of any of the SoxC genes in vitro promotes the generation of RGCs. Taken together, these data identify SOXC proteins as essential factors that promote the differentiation and maintain the survival of RGCs. This study provides insights into molecular networks underlying the course of retinal neurogenesis. Our results not only contribute to a better understanding of the genetic basis of RGC development, but also benefit the future translational research in developing new therapies to treat eye diseases related to RGC degeneration.

ISBN: 9781303504983Subjects--Topical Terms:

522710
Biology.

Regulation of Mouse Retinal Ganglion Cell Development by Sox4 and Sox11.
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520 $a The proper functioning of the retina is contingent upon the correct generation of the major cell types. Elucidation of developmental processes that give rise to anatomically and functionally distinct populations is essential for us to understand the proper function of the retina. This work is aimed to identify and functionally characterize novel transcription regulators involved in the development of retinal ganglion cells (RGCs). RGCs are the only projection neurons in the retina. Loss of RGCs results in various retinal diseases, such as glaucoma and other optic neuropathies. However, the genetic program controlling RGC development is largely unknown. Here we show that wide expression of the SoxC genes, Sox4 and Sox11, was observed throughout retinogenesis, particularly with high levels in the ganglion cell layer in an overlapping manner. To test the function of Sox4 and Sox11 in the development of mouse RGCs, we generated Sox4, Sox11 and Sox4/Sox11 conditional knockout (CKO) mice. Although targeted disruption of either Sox4 or Sox11 in retinas led to a mild reduction in the number of RGCs, combined deletion of Sox4 and Sox11 in the retina resulted in an abolishment of RGCs. Our developmental analysis demonstrates that Sox4 and Sox11 function redundantly to regulate the generation of RGCs at early embryonic stages as well as the survival of RGCs at late embryonic stages. Furthermore, genetic analysis reveals that Sox4 and Sox11 function between Math5 and Brn3b in the RGC regulatory pathway. In addition, overexpression of any of the SoxC genes in vitro promotes the generation of RGCs. Taken together, these data identify SOXC proteins as essential factors that promote the differentiation and maintain the survival of RGCs. This study provides insights into molecular networks underlying the course of retinal neurogenesis. Our results not only contribute to a better understanding of the genetic basis of RGC development, but also benefit the future translational research in developing new therapies to treat eye diseases related to RGC degeneration.
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