Dynamic regulation of SCG10 in regenerating axons after injury.
Peripheral axons can re-extend robustly after nerve injury. Soon after a nerve crush regenerating axons grow through the nerve segment distal to the lesion in close proximity to distal axons that are still morphologically and molecularly preserved. Hence, following the progress of regenerating axons necessitates markers that can distinguish between regenerating and degenerating axons. Here, we show that axonal levels of superior cervical ganglion 10 (SCG10) are dynamically regulated after axonal injury and provide an efficient method to label regenerating axons. In contrast to the rapid loss of SCG10 in distal axons (Shin et al., 2012b), we report that SCG10 accumulates in the proximal axons within an hour after injury, leading to a rapid identification of the lesion site. The increase in SCG10 levels is maintained during axon regeneration after nerve crush or nerve repair and allows for more selective labeling of regenerating axons than the commonly used markers growth-associated protein 43 (GAP43) and YFP. SCG10 is preferentially expressed in regenerating sensory axons rather than motor axons in the sciatic nerve. In a mouse model of slow Wallerian degeneration, SCG10 labeling remains selective for regenerating axons and allows for a quantitative analysis of delayed regeneration in this mutant. Taken together, these data demonstrate the utility of SCG10 as an efficient and selective marker of sensory axon regeneration.
Department of Developmental Biology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: jeshin@wustl.edu.
Jung Eun
JE
Shin
Department of Developmental Biology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: geislers@neuro.wustl.edu.
Stefanie
S
Geisler
Department of Developmental Biology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: diantonio@wustl.edu.
Aaron
A
DiAntonio
D000818:Animals; D001369:Axons / Q000378:metabolism / Q000473:pathology; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D002135:Calcium-Binding Proteins; D002478:Cells, Cultured; D002795:Choline O-Acetyltransferase / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D004622:Embryo, Mammalian; D019922:GAP-43 Protein / Q000378:metabolism; D005727:Ganglia, Spinal / Q000166:cytology; D005786:Gene Expression Regulation / Q000502:physiology*; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D008164:Luminescent Proteins / Q000235:genetics / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D008840:Microfilament Proteins / Q000235:genetics; D009416:Nerve Regeneration / Q000502:physiology*; D009612:Nicotinamide-Nucleotide Adenylyltransferase / Q000235:genetics / Q000378:metabolism; D012584:Sciatic Nerve / Q000378:metabolism / Q000473:pathology; D020426:Sciatic Neuropathy / Q000378:metabolism* / Q000503:physiopathology*; D050777:Stathmin; D013997:Time Factors; D014404:Tubulin / Q000378:metabolism
C113762:Avil protein, mouse; D001426:Bacterial Proteins; D002135:Calcium-Binding Proteins; D019922:GAP-43 Protein; D047908:Intracellular Signaling Peptides and Proteins; D008164:Luminescent Proteins; D008840:Microfilament Proteins; D050777:Stathmin; C512849:Stmn2 protein, mouse; D014404:Tubulin; C462941:beta3 tubulin, mouse; C054562:yellow fluorescent protein, Bacteria; D002795:Choline O-Acetyltransferase; D009612:Nicotinamide-Nucleotide Adenylyltransferase; C510972:Nmnat1 protein, mouse
Axon regeneration; Dorsal root ganglia (DRG); Marker of regenerating axon; NMNAT; Nerve repair; STMN2