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WIREs Dev Biol
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Timing of neuronal plasticity in development and aging

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Molecular oscillators are well known for their roles in temporal control of some biological processes like cell proliferation, but molecular mechanisms that provide temporal control of differentiation and postdifferentiation events in cells are less understood. In the nervous system, establishment of neuronal connectivity during development and decline in neuronal plasticity during aging are regulated with temporal precision, but the timing mechanisms are largely unknown. Caenorhabditis elegans has been a preferred model for aging research and recently emerges as a new model for the study of developmental and postdevelopmental plasticity in neurons. In this review we discuss the emerging mechanisms in timing of developmental lineage progression, axon growth and pathfinding, synapse formation, and reorganization, and neuronal plasticity in development and aging. We also provide a current view on the conserved core axon regeneration molecules with the intention to point out potential regulatory points of temporal controls. We highlight recent progress in understanding timing mechanisms that regulate decline in regenerative capacity, including progressive changes of intrinsic timers and co‐opting the aging pathway molecules. WIREs Dev Biol 2018, 7:e305. doi: 10.1002/wdev.305

This article is categorized under:

  • Invertebrate Organogenesis > Worms
  • Establishment of Spatial and Temporal Patterns > Regulation of Size, Proportion, and Timing
  • Nervous System Development > Worms
  • Gene Expression and Transcriptional Hierarchies > Regulatory RNA
Pathways regulating age‐related decline in neuronal regeneration in Caenorhabditis elegans. (a) The neuronal timers, let‐7 and lin‐41, signal developmental, and age‐related decline in neuronal regeneration as animals age. lin‐41 levels decline with advanced adult stage even though let‐7 levels also decline, suggesting that lin‐41 levels are likely regulated by both posttranscriptional (through the let‐7 and lin‐41 3′UTR interaction) and transcriptional (through the lin‐41 5′UTR) mechanisms in adult stage. (b) The aging pathway involving daf‐2, daf‐16, and fkh‐9 that was known to regulate organism longevity also influenced axon regeneration decline in aging.
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let‐7 mutations and lin‐41 overexpression restore regenerative capability in aged neurons. Neuronal regeneration capacity changes throughout the lifespan and diminishes with age. Inhibition of let‐7 miRNA or overexpression of its target, lin‐41, in aged neurons restores youthful regenerative capacity. Dashed blue lines represent detached axons affected by degeneration. Solid blue lines indicate newly regenerated axons.
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Gene Expression and Transcriptional Hierarchies > Regulatory RNA
Invertebrate Organogenesis > Worms
Establishment of Spatial and Temporal Patterns > Regulation of Size, Proportion, and Timing
Nervous System Development > Worms