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author:("eustar, Anne")
1.  Sp1 modifies leg-to-wing transdetermination in Drosophila 
Developmental biology  2012;373(2):290-299.
During Drosophila development, the transcription factor Sp1 is necessary for proper leg growth and also to repress wing development. Here we test the role of Sp1 during imaginal disc regeneration. Ubiquitous expression of wg induces a regeneration blastema in the dorsal aspect of the leg disc. Within this outgrowth, the wing selector gene vg is activated in some cells, changing their fate to wing identity in a process known as transdetermination. In this report we demonstrate that reducing the gene copy number of Sp1 significantly increases both the frequency and the area of transdetermination in regenerating leg discs. By examining the expression of known Sp1 target genes, we also show that the proximo-distal patterning gene dachshund is downregulated dorsally, leading to a break in its normal ring-shaped expression pattern. We further report that transdetermination, as evidenced by Vg expression, is only observed when there is a broken ring of Dachshund expression. Combined, these studies establish a role for Sp1 in leg-to-wing transdetermination.
doi:10.1016/j.ydbio.2012.11.008
PMCID: PMC3557525  PMID: 23165292
Imaginal disc; regeneration; transdetermination; selector gene; dachshund
2.  Drosophila twin spot clones reveal cell division dynamics in regenerating imaginal discs 
Developmental biology  2011;356(2):576-587.
Cell proliferation is required for tissue regeneration, yet the dynamics of proliferation during regeneration are not well understood. Here we investigated the proliferation of eye and leg regeneration in fragments of Drosophila imaginal discs. Using twin spot clones, we followed the proliferation and fates of sister cells arising from the same mother cell in the regeneration blastema. We show that the mother cell gives rise to two sisters that participate equally in regeneration. However, when cells switch disc identity and transdetermine to another fate, they fail to turn off the cell cycle and continue dividing long after regeneration is complete. We further demonstrate that the regeneration blastema moves as a sweep of proliferation, in which cells are displaced. Our results suggest that regenerating cells stop dividing once the missing parts are formed, but if they undergo a switch in cell fate, the proliferation clock is reset.
doi:10.1016/j.ydbio.2011.06.018
PMCID: PMC3144724  PMID: 21722631
regeneration; transdetermination; cell cycle; somatic cell immortality
3.  REGENERATION AND TRANSDETERMINATION: THE ROLE OF WINGLESS AND ITS REGULATION 
Developmental biology  2010;347(2):315-324.
SUMMARY
Imaginal discs of Drosophila have the remarkable ability to regenerate. After fragmentation wound healing occurs, ectopic wg is induced and a blastema is formed. In some, but not all fragments, the blastema will replace missing structures and a few cells can become more plastic and transdetermine to structures of other discs. A series of systematic cuts through the first leg disc revealed that a cut must transect the dorsal-proximal disc area and that the fragment must also include wg-competent cells. Fragments that fail to both transdetermine and regenerate missing structures will do both when provided with exogenous Wg, demonstrating the necessity of Wg in regenerative processes. In intact leg discs ubiquitously expressed low levels of Wg also leads to blastema formation, regeneration and transdetermination. Two days after exogenous wg induction the endogenous gene is activated, leading to elevated levels of Wg in the dorsal aspect of the leg disc. We identified a wg enhancer that regulates ectopic wg expression. Deletion of this enhancer increases transdetermination, but lowers the amount of ectopic Wg. We speculate that this lessens repression of dpp dorsally, and thus creates a permissive condition under which the balance of ectopic Wg and Dpp is favorable for transdetermination.
doi:10.1016/j.ydbio.2010.08.034
PMCID: PMC2976676  PMID: 20816798
4.  The Twin Spot Generator for differential Drosophila lineage analysis 
Nature methods  2009;6(8):600-602.
In Drosophila, widely-used mitotic recombination-based strategies generate mosaic flies with positive readout for only one daughter cell after division. To differentially label both daughter cells, we developed the Twin Spot Generator technique (TSG) and demonstrate that through mitotic recombination, TSG generates green and red twin spots in internal fly tissues, visible even as single cells. We discuss the wide applications of TSG to lineage and genetic mosaic studies.
doi:10.1038/nmeth.1349
PMCID: PMC2720837  PMID: 19633664
5.  Three genes control the timing, the site and the size of blastema formation in Drosophila 
Developmental biology  2008;319(1):68-77.
Regeneration is a vital process to maintain and repair tissues. Despite the importance of regeneration, the genes responsible for regenerative growth remain largely unknown. In Drosophila, imaginal disc regeneration can be induced either by fragmentation and in vivo culture or in situ by ubiquitous expression of wingless (wg/wnt1). Imaginal discs, like appendages in lower vertebrates, initiate regeneration by wound healing and proliferation at the wound site, forming a regeneration blastema. Most blastema cells maintain their disc-specific identity during regeneration; a few cells however, exhibit stem-cell like properties and switch to a different fate, in a phenomenon known as transdetermination. We identified three genes, regeneration (rgn), augmenter of liver regeneration (alr) and Matrix metalloproteinase-1 (Mmp1) expressed specifically in blastema cells during disc regeneration. Mutations in these genes affect both fragmentation- and wg-induced regeneration by either delaying, reducing or positioning the regeneration blastema. In addition to the modifications of blastema homeostasis, mutations in the three genes alter the rate of regeneration-induced transdetermination. We propose that these genes function in regenerative proliferation, growth and regulate cellular plasticity.
doi:10.1016/j.ydbio.2008.04.004
PMCID: PMC2483308  PMID: 18485344

Results 1-5 (5)