期刊
DEVELOPMENTAL BIOLOGY
卷 360, 期 2, 页码 286-296出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2011.09.015
关键词
Fat body; Tissue remodeling; 20E signaling; beta FTZ-F1; Matrix metalloproteinase
资金
- National Science Foundation (NSF) [IOS-0719591]
- University of Nevada, Las Vegas
- NSF RUI [0110238]
- NSF MRI [DBI-0216242]
- Howard Hughes Medical Institute (HHMI) [52005134]
- Div Of Molecular and Cellular Bioscience
- Direct For Biological Sciences [0110238] Funding Source: National Science Foundation
During metamorphosis, holometabolous insects eliminate obsolete larval tissues via programmed cell death. In contrast, tissues required for further development are retained and often remodeled to meet the needs of the adult fly. The larval fat body is involved in fueling metamorphosis, and thus it escapes cell death and is instead remodeled during prepupal development. The molecular mechanisms by which the fat body escapes programmed cell death have not yet been described, but it has been established that fat-body remodeling requires 20-hydroxyecdysone (20E) signaling. We have determined that 20E signaling is required within the fat body for the cell-shape changes and cell detachment that are characteristic of fat-body remodeling. We demonstrate that the nuclear hormone receptor beta FTZ-F1 is a key modulator of 20E hormonal induction of fat body remodeling and Matrix metalloproteinase 2 (MMP2) expression in the fat body. We show that induction of MMP2 expression in the fat body requires 20E signaling, and that MMP2 is necessary and sufficient to induce fat-body remodeling. (C) 2011 Elsevier Inc. All rights reserved.
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