The role of Inhibitor of Apoptosis in Fat Body Remodeling in Dr
Date
2011-05-23
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Abstract
The metamorphosis of Drosophila melanogaster results in destruction of many larval tissues by programmed cell death (PCD). PCD is regulated by the steroid hormone 20-hydroxyecdysone (ecdysone) (Yin et al., 2007). PCD is initiated by down-regulation of the antiapoptotic gene Inhibitor of Apoptosis (diap1). DIAP1 regulates PCD by inactivating caspases. Proapoptotic genes suppress diap1 to initiate histolysis of most larval tissues. A unique exception is the fat body, which instead of PCD undergoes remodeling from an organized tissue to a loose association of individual cells (Nelliot et al., 2006).
The timing of fat body remodeling is ecdysone-dependent, but its genetic regulation still needs to be elucidated. I hypothesize that the fat tissue is refractory to PCD due to upregulation of diap1. To test this hypothesis, I constructed a temporal profile of diap1 expression in fat body via quantitative Real Time PCR (qPCR). Additionally, I investigated if diap1 is necessary for fat body remodeling by studying fat body development in tissue specific loss-of-function diap1 animals. Here, I demonstrate that diap1 is upregulated throughout prepupal and early pupal development. While diap1 is not essential for fat body survival, diap1 appears essential for normal timing of fat body remodeling and pupal viability.
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Fat body remodeling, Drosophila melanogaster