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Developmental decline in neuronal regeneration by the progressive change of two intrinsic timers

Yan Zou1, Hui Chiu1, Anna Zinovyeva2

  • 1Division of Developmental Biology, Cincinnati Children's Hospital Research Foundation, Cincinnati, Ohio 45229.

Science (New York, N.Y.)
|April 20, 2013
PubMed

Insights

Aging Caenorhabditis elegans neurons lose axon regeneration ability due to the let-7 microRNA inhibiting LIN-41. This reciprocal let-7-LIN-41 circuit ensures regeneration is blocked only in older neurons.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Axon regeneration ability declines with age in both mammalian and Caenorhabditis elegans neurons.
  • The underlying molecular mechanisms for this age-dependent loss of regeneration are not fully understood.

Purpose of the Study:

  • To investigate the role of the let-7 microRNA in the age-related decline of anterior ventral microtubule (AVM) axon regeneration in Caenorhabditis elegans.
  • To elucidate the regulatory circuit controlling axon regeneration in aging neurons.

Main Methods:

  • Analysis of let-7 microRNA function in aging Caenorhabditis elegans neurons.
  • Investigating the interaction between let-7 and the LIN-41 protein.
  • Utilizing the 3' untranslated region of lin-41 and Argonaute ALG-1 in regulatory mechanisms.

Main Results:

  • let-7 microRNA inhibits AVM axon regeneration in older neurons by down-regulating LIN-41, a regeneration-promoting factor.
  • A reciprocal inhibitory circuit exists: let-7 inhibits lin-41 in older neurons, while LIN-41 inhibits let-7 in younger neurons via Argonaute ALG-1.
  • This circuit ensures that axon regeneration is specifically inhibited in older neurons.

Conclusions:

  • A let-7-LIN-41 regulatory circuit is repurposed in postmitotic neurons to control post-differentiation events, specifically axon regeneration.
  • This molecular mechanism explains the age-dependent decline in axon regeneration observed in Caenorhabditis elegans.
  • Findings highlight conserved regulatory mechanisms across different cell types and developmental stages.

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