TY  - GEN
T1  - Acute exposure of Nicotine during Drosophila puncture injury activates an epidermal wound response reaction.
AU  - Cherenfant, Chrissy
AU  - Juarez, Michelle T
DO  - 10.17912/micropub.biology.000415
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000415/
AB  - Biological model organisms provide an excellent in vivo system to test the effects of chemical exposure on developmental pathways. Recent studies in fruit fly Drosophila melanogaster highlight the strength of combining genetic screens and chemical inhibitors to dissect complex processes that promote an epidermal wound response during embryonic puncture injury assays (Juarez et al. 2011). The epidermal wound response reporter is based on the transcriptional reactivation of barrier formation genes, Dopa Decarboxylase (Ddc) and tyrosine hydroxylase (ple) in a localized pattern of cells that surround the site of injury (Juarez 2016). These genes each display their respective transcriptional expression phenotypes in epidermal cells: local gene activation is limited to the cells surrounding the site of damage in wild type genetic backgrounds and global gene activation is unlimited and spreads beyond the cells surrounding the site of damage in immune response mutants (e.g. Flotillin-2 and Toll) (Juarez et al. 2011; Patterson et al. 2013). The epidermal wound response reporter is based on the characterization of a transgenic enhancer sequence that activates green fluorescence protein (GFP) in a wound-dependent and epidermal-specific pattern localized in the cells that surround the site of injury, referred to as Ddc-GFP (Juarez 2016). Fundamentally, the fluorescent reporter provides an in-vivo tool for visualizing the wound reaction caused by epidermal injury.
PY  - 2021
JO  - microPublication Biology
ER  -