The Abl/enabled signaling pathway regulates Golgi architecture in Drosophila photoreceptor neurons.
Bottom Line: The Abl effector, Enabled (Ena), selectively labels the cis-Golgi in developing PRs.Finally, we demonstrate that the effects of Abl signaling on Golgi are mediated via regulation of the actin cytoskeleton.Moreover, they raise the possibility that some of the effects of Abl signaling may arise, in part, from alterations of protein trafficking and secretion.
Affiliation: Axon Guidance and Neural Connectivity Unit, Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.Show MeSH
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Mentions: The number and subcellular distribution of Golgi cisternae were profoundly sensitive to the level of Ena protein (Figures 2, A– F, and 3, D and E). In WT we found 3.8 ± 1.0 cis-Golgi cisternae (GM130 positive; mean ± SEM) and 5.5 ± 1.2 trans-Golgi (dSyx-16 positive) per PR cell body scattered more or less evenly across the soma (Figures 2, A and E, and 3, A and F), with 45.6% ± 2.1 of cis-Golgi and 50.3% ± 1.9 of trans-Golgi in the basal half of the cell and the rest apical (Figures 2F and 3G). In contrast, when we overexpressed an Ena-GFP fusion, the number of distinguishable cisternae increased dramatically (to 8.6 ± 1.1 cis-Golgi, p = 2.1E-5; and 15.7 ± 0.9 trans-Golgi; p = 2.7E-4; Figures 2E and 3F), and the cisternae overwhelmingly relocalized to the most basal part of the cell soma, near the axon exit point (cis-Golgi, 97.5% ± 3.3 basal, p = 2.3E-4; and trans-Golgi, 79% ± 4.6 basal; p = 2.6E-5; Figures 2F and 3G). Both the expressed and the endogenous Ena relocalized in concert with the Golgi, coalescing at the most basal point of the cell soma (Figures 2B and 3D). We verified that the phenotype from ena overexpression was formally a genetic gain of function by showing that the severity of the phenotype was quantitatively reduced by heterozygosity for the endogenous ena locus (Figure S2, D and E).
Affiliation: Axon Guidance and Neural Connectivity Unit, Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.