Dauer-specific dendrite arborization in C. elegans is regulated by KPC-1/Furin.
BACKGROUND
Dendrites often display remarkably complex and diverse morphologies that are influenced by developmental and environmental cues. Neuroplasticity in response to adverse environmental conditions entails both hypertrophy and resorption of dendrites. How dendrites rapidly alter morphology in response to unfavorable environmental conditions is unclear. The nematode Caenorhabditis elegans enters into a stress-resistant dauer larval stage in response to an adverse environment.


RESULTS
Here we show that the IL2 bipolar sensory neurons undergo dendrite arborization and axon remodeling during dauer development. When dauer larvae are returned to favorable environmental conditions, animals resume reproductive development and IL2 dendritic branches retract, leaving behind remnant branches in postdauer L4 and adult animals. The C. elegans furin homolog KPC-1 is required for dauer IL2 dendritic arborization and dauer-specific nictation behavior. KPC-1 is also necessary for dendritic arborization of PVD and FLP sensory neurons. In mammals, furin is essential, ubiquitously expressed, and associated with numerous pathologies, including neurodegenerative diseases. While broadly expressed in C. elegans neurons and epithelia, KPC-1 acts cell autonomously in IL2 neurons to regulate dauer-specific dendritic arborization and nictation.


CONCLUSIONS
Neuroplasticity of the C. elegans IL2 sensory neurons provides a paradigm to study stress-induced and reversible dendritic branching, and the role of environmental and developmental cues in this process. The newly discovered role of KPC-1 in dendrite morphogenesis provides insight into the function of proprotein convertases in nervous system development.
Department of Genetics and The Human Genetics Institute of New Jersey, Rutgers University, 145 Bevier Road, Piscataway, NJ 08854 USA.
Nathan E
NE
Schroeder
Rebecca J
RJ
Androwski
Alina
A
Rashid
Harksun
H
Lee
Junho
J
Lee
Maureen M
MM
Barr
D000818:Animals; D030801:Animals, Genetically Modified / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D017173:Caenorhabditis elegans / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics* / Q000378:metabolism; D003712:Dendrites / Q000502:physiology; D045683:Furin / Q000235:genetics* / Q000378:metabolism; D007814:Larva / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D018613:Microscopy, Confocal; D009043:Motor Activity; D009473:Neuronal Plasticity; D011984:Sensory Receptor Cells / Q000502:physiology
D029742:Caenorhabditis elegans Proteins; D045683:Furin