Journal: Disease Models & Mechanisms

Article Title: Mediators of a long-term movement abnormality in a Drosophila melanogaster model of classic galactosemia

doi: 10.1242/dmm.009050

Figure Lengend Snippet: GALT -null D. melanogaster show no apparent morphological defects in brain or muscle. (A) Representative images of adult brain (upper panels) and muscle tissue (lower panels) from GALT -null and control animals. Arrows in the brain images point to cortex, arrowheads point to vacuoles and the asterisk indicates normal neuropil. There were no apparent differences in gross anatomical structures between the GALT -null and control animals in either tissue. Scale bar: 20 μm. (B) Representative immunofluorescence stains for mitochondria using an antibody directed to ATP synthase reveals no clear abnormalities of mitochondrial structure or number in GALT -null neurons. A DAPI counterstain was used to stain nuclei. Scale bar: 5 μm. (C) Representative immunohistochemical stains for synapsin (SYN), the vesicular glutamate transporter (VGLUT) and the microtubule binding protein futsch revealed no clear defects in GALT -null animals. Scale bar: 40 μm.

Article Snippet: Immunostaining was performed using the following mouse monoclonal primary antibodies: anti-synapsin (Developmental Studies Hybridoma Bank), anti-vGlut (Feany laboratory), anti-futsch (Developmental Studies Hybridoma Bank) and anti-ATP synthase (MitoSciences).

Techniques: Control, Immunofluorescence, Staining, Immunohistochemical staining, Binding Assay