4.3 Article

Normal dendrite growth in Drosophila motor neurons requires the AP-1 transcription factor

Journal

DEVELOPMENTAL NEUROBIOLOGY
Volume 68, Issue 10, Pages 1225-1242

Publisher

WILEY
DOI: 10.1002/dneu.20655

Keywords

dendrites; Drosophila; AP-1; plasticity; development

Funding

  1. NCI NIH HHS [T32 CA009213, T32 CA09213] Funding Source: Medline
  2. NIDA NIH HHS [DA1333, K02 DA017749, KO2-DA017749] Funding Source: Medline
  3. NIGMS NIH HHS [T32 GM008400] Funding Source: Medline
  4. NINDS NIH HHS [NS057637, P01 NS028495, R01 NS057637-02, R01 NS057637, NS28495, R01 NS057637-01] Funding Source: Medline

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During learning and memory formation, information flow through networks is regulated significantly through structural alterations in neurons. Dendrites, sites of signal integration, are key targets of activity-mediated modifications. Although local mechanisms of dendritic growth ensure synapse-specific changes, global mechanisms linking neural activity to nuclear gene expression may have profound influences on neural function. Fos, being an immediate-early gene, is ideally suited to be an initial transducer of neural activity, but a precise role for the AP-1 transcription factor in dendrite growth remains to be elucidated. Here we measure changes in the dendritic fields of identified Drosophila motor neurons in vivo and in primary culture to investigate the role of the immediate-early transcription factor AP-1 in regulating endogenous and activity-induced dendrite growth. Our data indicate that (a) increased neural excitability or depolarization stimulates dendrite growth, (b) AP-1 (a Fos, Jun heterodimer) is required for normal motor neuron dendritic growth during development and in response to activity induction, and (c) neuronal Fos protein levels are rapidly but transiently induced in motor neurons following neural activity. Taken together, these results show that AP-1 mediated transcription is important for dendrite growth, and that neural activity influences global dendritic growth through a gene-expression dependent mechanism gated by AP-1. (c) 2008 Wiley Periodicals, Inc.

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