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In this study, I proposed that the ectopic expression of Bftz-fl in D. melanogaster third instar larvae during the first 20E pulse will trigger the premature expression of E93, resulting in premature fat body remodeling. My results to date have shown that ectopic expression of Bftz-f1 in third instar larva leads to premature expression of E93 and fat body remodeling. Transmission electron microscopy showed that autophagosomes are present in dissociating fat bodies suggesting that the fat body fuels the process of metamorphosis by releasing nutrients.
Tissue remodeling plays an important role in the development of many multicellular organisms. It is also a key process in wound healing and tumor metastasis, and studying the control of tissue remodeling could lead to important developments in medicine, such as treatment and prevention of cancer and other diseases. ​Drosophila melanogaster,​ more commonly known as the fruit fly, is a great model organism to study such processes, due to their short life cycle and genomic similarities to humans. When ​Drosophila​ develop from larva into adult flies, they undergo metamorphosis, in which most of the larval tissues are destroyed by programmed cell death and replaced by adult tissues. However, the larval fat body is exempt from such cell death and is maintained until a few days into adulthood. During metamorphosis, the larval fat body cells remodel structurally through detaching from one another and moving to the head cavity. The larval fat body remodeling is a critical process, as failure to do so leads to lethality. Past members of the Woodard Lab performed complementation tests on fly lines that each had a single mutation on the third chromosome that resulted in abnormal fat body morphology and pharate adult lethality. The current study focuses on line l(3)LL-15413:L 04 PA, one of the seven lines that were identified to have completely lost the ability to remodel fat bodies during metamorphosis. In order to identify the location of the mutation causing the loss of fat body remodeling, I used the mapping methodology developed by Sapiro et al. (2013), and was able to determine the approximate location of the mutation to be between the dominant marker pair, ​Stubble​ and ​Hairless.​ Following that, line l(3)LL-15413:L 04 PA was crossed with 13 deficiency stocks, each missing a small fragment of the third chromosome, to further narrow down the location of the mutation. Despite having the gene mapped between the two dominant markers, I was unable to find a deficiency line that uncovered the mutation gene. Further experiments are required to determine the exact location and role of this gene, as well as other lines with abnormal fat body morphology. I hope this study will be a groundwork for further studies in the field.
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"The old order changeth, yielding place to new. " When Tennyson wrote this, he was unfamiliar with the pace of modem science else he would have said the new is displaced by the newer. When Gilbert and I gathered the papers for the first edition of this overview of metamorphosis, we aimed to provide a broad basis upon which the experimental analysis of the developmental changes called metamorphosis could proceed. We were both aware then that with the new techniques of biochemistry and with the revolutionary breakthrough to the nature of the gene, countless new possibilities were being opened for the exploration of the molecular basis of development. The resources offered by metamorphic changes offered unique opportunities to trace the path from gene to phenotype. Our expectations were high. I visited Larry Gilbert and Earl Frieden in their laboratories and saw with envy how far advanced they were then in the use of molecular methods of analysis. I had started on a different approach to develop an in vitro test for thyroid action on amphibian tissue. But circumstances limited my own progress to the initial delim itation of the technical possibilities of the in vitro system. Only from the sidelines could I watch the steady if slow progress of biology in penetrating the maze of molecular events by which animal tissues re spond to hormonal and other developmental factors.
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.
Undergraduate honors thesis - Mount Holyoke College, 2016. Program in Biochemistry.
Past research has shown that ecdysone signaling cascades are required for fat body remodeling. During the second pulse of 20E, the most active form of ecdysone, both E93 and MMP2 are expressed. In my research I examine E93 loss-of-function mutants and wild type for expression of MMP2 transcripts in fat body to test the hypothesis that E93 regulates transcription levels of MMP2 during fat body remodeling in Drosophila melanogaster.
I hypothesized that diap1 is expressed in the larval fat body throughout metamorphosis and that this helps to inhibit PCD in this organ. To test this hypothesis, I examined diap1 transcript levels in wild type Drosophila using qPCR. In addition, I determined the expression of diap1 in larval fat body of flies with a diap1 RNAi construct. My results demonstrate that diap1 is expressed in the larval fat body during prepupal and early pupal development. Preliminary findings showed that Drosophila expressing the diap1 RNAi construct failed to undergo normal fat body remodeling. This finding suggests that diap1 is necessary for the normal timing of fat body remodeling and the successful development of Drosophila.
Matrix metalloproteinases are enzymes involved in important tissue remodeling mechanisms in many animal systems, including mammalian. They are required for scar resorption during wound healing, and are believed to also influence inflammation and re-epithelialization. MMPs work by loosening ECM contacts between cells at the wound edge, allowing uninjured cells behind the edge to proliferate and cover the damaged tissue (Gill and Parks, 2008). The proteases also take part in metastatic activity of tumor cells because they degrade the ECM of tumor cells, allowing them to detach and migrate to other parts of the body (Sato et al, 2005). In Drosophila, Matrix metalloproteinase 2 (MMP2) plays a vital role in tissue remodeling and programmed cell-death during metamorphosis (Page-McCaw, 2008). The larval fat body of Drosophila develops in the larva during the beginning stages of its life. This organ stores nutrients that power the animal through the non-feeding periods of its life, including metamorphosis. Metamorphosis is triggered by a pulse of 20-hydroxyecdysone (20E), which induces pupariation. 20E controls expression of dBlimp-1, a rapidly degrading protein that transcriptionally represses ßftz-f1. As the 20E titer declines, dBlimp-1 is degraded and the ßFTZ-F1 transcription factor is expressed (Agawa et al., 2007). ßFTZ-F1 functions as a nuclear receptor and confers competence upon tissues to be able to respond to a second pulse of 20E. MMP2 is expressed during the second pulse of 20E, and cleaves proteins in the ECM, enabling fat body cells to migrate. This second pulse induces the prepupal to pupal transition (Woodard et al., 1994). It has been shown that ßftz-f1 is necessary and sufficient to induce fat body remodeling in the presence of 20E. Without MMP2, the larval fat body fails to dissociate, and the transition does not occur normally (Bond, 2011). I am examining the regulation of MMP2 expression in larval fat body remodeling in D. melanogaster. I am testing the hypothesis that ßftz-f1 is necessary for the induction of MMP2 transcription by 20E in the late prepupa. I used transgenic flies to overexpress dBlimp-1 in the larval fat body, and examined the expression of MMP2 in the transgenic fat body compared to controls.