SDF1-induced antagonism of axonal repulsion requires multiple G-protein coupled signaling components that work in parallel.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21556147.
- Also identified by DOI 10.1371/journal.pone.0018896 and PMC identifier 3083402.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
SDF1 reduces the responsiveness of axonal growth cones to repellent guidance cues in a pertussis-toxin-sensitive, cAMP-dependent manner. Here, we show that SDF1's antirepellent effect can be blocked in embryonic chick dorsal root ganglia (DRGs) by expression of peptides or proteins inhibiting either Gα(i), Gα(q), or Gβγ. SDF1 antirepellent activity is also blocked by pharmacological inhibition of PLC, a common effector protein for Gα(q). We also show that SDF1 antirepellent activity can be mimicked by overexpression of constitutively active Gα(i), Gα(q), or Gα(s). These results suggest a model in which multiple G protein components cooperate to produce the cAMP levels required for SDF1 antirepellent activity.
Medical subject headings
- Axons
- Chemokine CXCL12
- GTP-Binding Proteins
- Signal Transduction