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The Abl/enabled signaling pathway regulates Golgi architecture in Drosophila photoreceptor neurons.

Kannan R, Kuzina I, Wincovitch S, Nowotarski SH, Giniger E - Mol. Biol. Cell (2014)

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.

View Article: PubMed Central - PubMed

Affiliation: Axon Guidance and Neural Connectivity Unit, Basic Neuroscience Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

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Coexpression of cpb and Ena rescues cis-Golgi phenotypes. (A) Overexpression of Ena alone. (B) Coexpression of Ena and cpb. (C) Overexpression of Cpb alone. Note that overexpression of cpb suppresses both fragmentation and basal localization of Golgi puncta and of Ena itself. (D) Single optical section of a wild-type eye disk stained for F-actin (phalloidin; green) and cis-Golgi (anti-GM130; red). Note accumulation of F-actin adjacent to many Golgi puncta. Some of the Golgi are adjacent to actin foci not visible in this focal plane. Elav (blue) marks PRs. (E) Quantification of Golgi apicobasal distribution for Ena and cpb coexpression experiment (A–C). (F) Quantification of Golgi fragmentation for Ena and Cpb coexpression experiments (A–C). n for each genotype is reported on the bars. Error bars represent SEM. **p < 0.001.
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Figure 6: Coexpression of cpb and Ena rescues cis-Golgi phenotypes. (A) Overexpression of Ena alone. (B) Coexpression of Ena and cpb. (C) Overexpression of Cpb alone. Note that overexpression of cpb suppresses both fragmentation and basal localization of Golgi puncta and of Ena itself. (D) Single optical section of a wild-type eye disk stained for F-actin (phalloidin; green) and cis-Golgi (anti-GM130; red). Note accumulation of F-actin adjacent to many Golgi puncta. Some of the Golgi are adjacent to actin foci not visible in this focal plane. Elav (blue) marks PRs. (E) Quantification of Golgi apicobasal distribution for Ena and cpb coexpression experiment (A–C). (F) Quantification of Golgi fragmentation for Ena and Cpb coexpression experiments (A–C). n for each genotype is reported on the bars. Error bars represent SEM. **p < 0.001.

Mentions: Genetic and pharmacological experiments suggest that Abl/Ena signaling controls Golgi distribution through its regulation of the actin cytoskeleton. Ena promotes actin filament assembly in part by blocking capping of the barbed ends of actin filaments (Bear et al., 2002). Thus capping protein-β (cpb) and Ena act antagonistically during Drosophila oogenesis (Gates et al., 2009) and axon patterning (Kuzina et al., 2011), with cpb genetically downstream of ena (Gates et al., 2009). We found that promoting actin capping by coexpressing cpb with ena significantly suppressed Ena-dependent basal accumulation of cis-Golgi (UAS-Ena, 98.3% ± 1.8 basal, vs. UAS-cpb + UAS-Ena, 43.8% ± 2.6 basal; not significantly different from WT, 43.4% ± 4.2 basal; Figure 6, A– C). Enhanced capping also suppressed Ena-dependent fragmentation of cis-Golgi cisternae in PR (UAS-Ena, 8.9 ± 1.3 fragments, vs. UAS-cpb + UAS-Ena, 3.9 ± 1.5 fragments; not significantly different from WT, 3.3 ± 1.0 fragments) (Figure 6F). Ena localization was also largely restored to the wild-type pattern by coexpressing cpb with ena (Figure 6B) compared with ena gain-of-function alone (Figure 6A). Overexpression of capping protein alone did not show any significant effects on Golgi distribution or Ena localization (Figure 6C), and co-overexpression of cpb did not noticeably alter the level of UAS-driven ena (as assessed by fluorescence intensity).


The Abl/enabled signaling pathway regulates Golgi architecture in Drosophila photoreceptor neurons.

Kannan R, Kuzina I, Wincovitch S, Nowotarski SH, Giniger E - Mol. Biol. Cell (2014)

Coexpression of cpb and Ena rescues cis-Golgi phenotypes. (A) Overexpression of Ena alone. (B) Coexpression of Ena and cpb. (C) Overexpression of Cpb alone. Note that overexpression of cpb suppresses both fragmentation and basal localization of Golgi puncta and of Ena itself. (D) Single optical section of a wild-type eye disk stained for F-actin (phalloidin; green) and cis-Golgi (anti-GM130; red). Note accumulation of F-actin adjacent to many Golgi puncta. Some of the Golgi are adjacent to actin foci not visible in this focal plane. Elav (blue) marks PRs. (E) Quantification of Golgi apicobasal distribution for Ena and cpb coexpression experiment (A–C). (F) Quantification of Golgi fragmentation for Ena and Cpb coexpression experiments (A–C). n for each genotype is reported on the bars. Error bars represent SEM. **p < 0.001.
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Figure 6: Coexpression of cpb and Ena rescues cis-Golgi phenotypes. (A) Overexpression of Ena alone. (B) Coexpression of Ena and cpb. (C) Overexpression of Cpb alone. Note that overexpression of cpb suppresses both fragmentation and basal localization of Golgi puncta and of Ena itself. (D) Single optical section of a wild-type eye disk stained for F-actin (phalloidin; green) and cis-Golgi (anti-GM130; red). Note accumulation of F-actin adjacent to many Golgi puncta. Some of the Golgi are adjacent to actin foci not visible in this focal plane. Elav (blue) marks PRs. (E) Quantification of Golgi apicobasal distribution for Ena and cpb coexpression experiment (A–C). (F) Quantification of Golgi fragmentation for Ena and Cpb coexpression experiments (A–C). n for each genotype is reported on the bars. Error bars represent SEM. **p < 0.001.
Mentions: Genetic and pharmacological experiments suggest that Abl/Ena signaling controls Golgi distribution through its regulation of the actin cytoskeleton. Ena promotes actin filament assembly in part by blocking capping of the barbed ends of actin filaments (Bear et al., 2002). Thus capping protein-β (cpb) and Ena act antagonistically during Drosophila oogenesis (Gates et al., 2009) and axon patterning (Kuzina et al., 2011), with cpb genetically downstream of ena (Gates et al., 2009). We found that promoting actin capping by coexpressing cpb with ena significantly suppressed Ena-dependent basal accumulation of cis-Golgi (UAS-Ena, 98.3% ± 1.8 basal, vs. UAS-cpb + UAS-Ena, 43.8% ± 2.6 basal; not significantly different from WT, 43.4% ± 4.2 basal; Figure 6, A– C). Enhanced capping also suppressed Ena-dependent fragmentation of cis-Golgi cisternae in PR (UAS-Ena, 8.9 ± 1.3 fragments, vs. UAS-cpb + UAS-Ena, 3.9 ± 1.5 fragments; not significantly different from WT, 3.3 ± 1.0 fragments) (Figure 6F). Ena localization was also largely restored to the wild-type pattern by coexpressing cpb with ena (Figure 6B) compared with ena gain-of-function alone (Figure 6A). Overexpression of capping protein alone did not show any significant effects on Golgi distribution or Ena localization (Figure 6C), and co-overexpression of cpb did not noticeably alter the level of UAS-driven ena (as assessed by fluorescence intensity).

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.

View Article: PubMed Central - PubMed

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
Related in: MedlinePlus