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: Live imaging of Golgi biogenesis using a Golgi marker, α-mannosidase II-eGFP, revealed that Abl controls the dynamics of Golgi fusion and fission events in vivo (Figure 5, A– C, and Supplemental Movies S1 and S2). In wild-type PR neurons, small clusters consisting of vesicular and tubular-shaped Golgi structures were present throughout the cell. They were highly dynamic and exhibited stochastic movement in both apical and basal directions. We also observed selective fusion of neighboring vesicular structures, eventually leading to the formation of tubular-shaped Golgi, as well as to fission of preexisting Golgi structures (Figure 5A and Supplemental Movie S1). Fusion and fission events were not synchronous for all Golgi structures in the same cell. In Abl mutants (Figure 5B and Supplemental Movie S2), Golgi exhibit restricted movement compared with the dynamics observed in wild type (Figure 5A), with Golgi puncta staying more aggregated in the vicinity of their neighbors. Moreover, counting fission and fusion events revealed a significant increase in fission and decrease in fusion of Golgi fragments per unit time in Abl mutants compared with wild type. In WT eye disks, we observed 3.6 ± 0.8 apparent fission events and 4.9 ± 0.3 fusion events per PR cluster per 15.6-s observation period (as assessed morphologically, at the resolution of spinning disk confocal imaging). In contrast, Abl mutants showed 6.8 ± 0.4 apparent fission events (p = 1.8E-07) and 2.4 ± 0.9 fusion events per cluster (p = 2.1E-08). Thus it appears that Abl activity promotes fusion and limits fission of Golgi fragments in PR neurons (Figure 5C).
Affiliation: Axon Guidance and Neural Connectivity Unit, Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.