語系:
繁體中文
English
說明(常見問題)
回圖書館首頁
手機版館藏查詢
登入
回首頁
切換:
標籤
|
MARC模式
|
ISBD
Circadian genes are necessary for sk...
~
Andrews, Jessica L.
FindBook
Google Book
Amazon
博客來
Circadian genes are necessary for skeletal muscle function and phenotype.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Circadian genes are necessary for skeletal muscle function and phenotype./
作者:
Andrews, Jessica L.
面頁冊數:
154 p.
附註:
Adviser: Karyn A. Esser.
Contained By:
Dissertation Abstracts International68-06B.
標題:
Biology, Physiology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3266950
ISBN:
9780549052098
Circadian genes are necessary for skeletal muscle function and phenotype.
Andrews, Jessica L.
Circadian genes are necessary for skeletal muscle function and phenotype.
- 154 p.
Adviser: Karyn A. Esser.
Thesis (Ph.D.)--University of Illinois at Chicago, Health Sciences Center, 2007.
An endogenous central clock in the brain, coupled to the environmental light cycle, drives circadian rhythms of behavior and physiology. Circadian rhythm of core clock gene expression occur widely in peripheral tissues such as liver, heart and skeletal muscle. One of the ongoing questions in circadian biology is how these core clock genes regulate tissue specific processes. Much of the research has focused on liver, heart, and kidney with skeletal muscle receiving no attention. We show here that in both Clock mutant and Bmal1-/- mice there was and a significant deficit in skeletal muscle force production, reduction in mitochondrial volume density, and alteration in mitochondrial ultrastructure. Thus it appears that an intact molecular clock is necessary for maintenance of both skeletal muscle structure and function. Expression profiling of skeletal muscle mRNA was performed with the aim of identifying genes that may link altered core clock function with force deficits and mitochondrial impairments in skeletal muscle. Analysis of gene array results identified MyoD1 and Pgc-1beta as being expressed in a circadian fashion in skeletal muscle of wildtype mice while remaining non-cyclic and suppressed in the skeletal muscle of Clock mutant mice. Furthermore, measurements of maximal isometric force production in the EDL of MyoD1-/- mice revealed a 30% force deficit, similar to the deficit observed in the Clock mutant and Bmal1-/- mice. These results suggest that a disruption in the core clock mechanism is responsible for the lost and/or mis-expression of MyoD1 and Pgc-1beta, potentially contributing to the observed deficit in force production and loss in mitochondrial volume, respectively. To determine the necessity of Bmal1 expression in regulating mitochondrial function, respiration was measured in the mitochondria isolated from the diaphragm and gastrocnemius of 12 week old Bmal1-/- and wildtype mice. A significant reduction in mitochondrial efficiency and increase in oxidant activity, in the skeletal muscle of Bmal1-/- mice, suggests that Bmal1 is necessary for the maintenance of mitochondrial function and oxidant balance.
ISBN: 9780549052098Subjects--Topical Terms:
1017816
Biology, Physiology.
Circadian genes are necessary for skeletal muscle function and phenotype.
LDR
:03048nam 2200265 a 45
001
943683
005
20110520
008
110520s2007 ||||||||||||||||| ||eng d
020
$a
9780549052098
035
$a
(UMI)AAI3266950
035
$a
AAI3266950
040
$a
UMI
$c
UMI
100
1
$a
Andrews, Jessica L.
$3
1267717
245
1 0
$a
Circadian genes are necessary for skeletal muscle function and phenotype.
300
$a
154 p.
500
$a
Adviser: Karyn A. Esser.
500
$a
Source: Dissertation Abstracts International, Volume: 68-06, Section: B, page: 3603.
502
$a
Thesis (Ph.D.)--University of Illinois at Chicago, Health Sciences Center, 2007.
520
$a
An endogenous central clock in the brain, coupled to the environmental light cycle, drives circadian rhythms of behavior and physiology. Circadian rhythm of core clock gene expression occur widely in peripheral tissues such as liver, heart and skeletal muscle. One of the ongoing questions in circadian biology is how these core clock genes regulate tissue specific processes. Much of the research has focused on liver, heart, and kidney with skeletal muscle receiving no attention. We show here that in both Clock mutant and Bmal1-/- mice there was and a significant deficit in skeletal muscle force production, reduction in mitochondrial volume density, and alteration in mitochondrial ultrastructure. Thus it appears that an intact molecular clock is necessary for maintenance of both skeletal muscle structure and function. Expression profiling of skeletal muscle mRNA was performed with the aim of identifying genes that may link altered core clock function with force deficits and mitochondrial impairments in skeletal muscle. Analysis of gene array results identified MyoD1 and Pgc-1beta as being expressed in a circadian fashion in skeletal muscle of wildtype mice while remaining non-cyclic and suppressed in the skeletal muscle of Clock mutant mice. Furthermore, measurements of maximal isometric force production in the EDL of MyoD1-/- mice revealed a 30% force deficit, similar to the deficit observed in the Clock mutant and Bmal1-/- mice. These results suggest that a disruption in the core clock mechanism is responsible for the lost and/or mis-expression of MyoD1 and Pgc-1beta, potentially contributing to the observed deficit in force production and loss in mitochondrial volume, respectively. To determine the necessity of Bmal1 expression in regulating mitochondrial function, respiration was measured in the mitochondria isolated from the diaphragm and gastrocnemius of 12 week old Bmal1-/- and wildtype mice. A significant reduction in mitochondrial efficiency and increase in oxidant activity, in the skeletal muscle of Bmal1-/- mice, suggests that Bmal1 is necessary for the maintenance of mitochondrial function and oxidant balance.
590
$a
School code: 0806.
650
4
$a
Biology, Physiology.
$3
1017816
690
$a
0719
710
2
$a
University of Illinois at Chicago, Health Sciences Center.
$3
1021703
773
0
$t
Dissertation Abstracts International
$g
68-06B.
790
$a
0806
790
1 0
$a
Esser, Karyn A.,
$e
advisor
791
$a
Ph.D.
792
$a
2007
856
4 0
$u
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3266950
筆 0 讀者評論
館藏地:
全部
電子資源
出版年:
卷號:
館藏
1 筆 • 頁數 1 •
1
條碼號
典藏地名稱
館藏流通類別
資料類型
索書號
使用類型
借閱狀態
預約狀態
備註欄
附件
W9113324
電子資源
11.線上閱覽_V
電子書
EB W9113324
一般使用(Normal)
在架
0
1 筆 • 頁數 1 •
1
多媒體
評論
新增評論
分享你的心得
Export
取書館
處理中
...
變更密碼
登入