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UNC-16/JIP3 negatively regulates actin dynamics dependent on DLK-1 and microtubule dynamics independent of DLK-1 in regenerating neurons
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Abstract
Neuronal regeneration after injury depends on the intrinsic growth potential of neurons. UNC-16, a
C. elegans
JIP3 homologue, inhibits axonal regeneration by regulating regrowth initiation and rate of regrowth. UNC-16/JIP3 inhibits the regeneration promoting activity of DLK-1 long but acts additively to and independently of inhibitory DLK-1 short isoform. UNC-16/JIP3 promotes DLK-1 punctate localization in a concentration dependent manner limiting DLK-1 long availability at the cut site minutes after injury. UNC-16 negatively regulates actin dynamics dependent on DLK-1 and microtubule dynamics independent of DLK-1. The faster regeneration seen in
unc-16
does not lead to functional recovery. We propose a model where UNC-16/JIP3 plays its inhibitory role through tight temporal and spatial control of DLK-1 function. The dual inhibitory control by both UNC-16 and DLK-1 short calibrate the intrinsic growth promoting function of DLK-1 long in vivo.
Title: UNC-16/JIP3 negatively regulates actin dynamics dependent on DLK-1 and microtubule dynamics independent of DLK-1 in regenerating neurons
Description:
Abstract
Neuronal regeneration after injury depends on the intrinsic growth potential of neurons.
UNC-16, a
C.
elegans
JIP3 homologue, inhibits axonal regeneration by regulating regrowth initiation and rate of regrowth.
UNC-16/JIP3 inhibits the regeneration promoting activity of DLK-1 long but acts additively to and independently of inhibitory DLK-1 short isoform.
UNC-16/JIP3 promotes DLK-1 punctate localization in a concentration dependent manner limiting DLK-1 long availability at the cut site minutes after injury.
UNC-16 negatively regulates actin dynamics dependent on DLK-1 and microtubule dynamics independent of DLK-1.
The faster regeneration seen in
unc-16
does not lead to functional recovery.
We propose a model where UNC-16/JIP3 plays its inhibitory role through tight temporal and spatial control of DLK-1 function.
The dual inhibitory control by both UNC-16 and DLK-1 short calibrate the intrinsic growth promoting function of DLK-1 long in vivo.
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