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Published November 18, 2004 | Supplemental Material
Journal Article Open

The Translational Repressor Pumilio Regulates Presynaptic Morphology and Controls Postsynaptic Accumulation of Translation Factor eIF-4E


Translational repression by Drosophila Pumilio (Pum) protein controls posterior patterning during embryonic development. Here, we show that Pum is an important mediator of synaptic growth and plasticity at the neuromuscular junction (NMJ). Pum is localized to the postsynaptic side of the NMJ in third instar larvae and is also expressed in larval neurons. Neuronal Pum regulates synaptic growth. In its absence, NMJ boutons are larger and fewer in number, while Pum overexpression increases bouton number and decreases bouton size. Postsynaptic Pum negatively regulates expression of the translation factor eIF-4E at the NMJ, and Pum binds selectively to the 3′UTR of eIF-4E mRNA. The GluRIIa glutamate receptor is upregulated in pum mutants. These results, together with genetic epistasis studies, suggest that postsynaptic Pum modulates synaptic function via direct control of eIF-4E expression.

Additional Information

© 2004 Elsevier B.V. Received 5 November 2003, Revised 26 June 2004, Accepted 6 October 2004, Available online 17 November 2004. Published: November 17, 2004. We thank the members of the Zinn group and Erin Schuman, Christoph Schuster, Aaron DiAntonio, Chand Desai, and Ruth Lehmann for helpful discussions. We thank Thomas Osterwalder and Haig Keshishian for GeneSwitch flies; Christoph Schuster and Paul Lasko for eIF-4E antibody and transgenic lines; Ruth Lehmann for anti-PumN; Yoshiaki Kidokoro for GluRIIa antibody; Aaron DiAntonio for GluRIIB and GluRIII antibodies; Dan Woods and Peter Bryant for Discs-large antibody; Murim Choi for making the Pum transgenic lines; Anna Salazar, Elena Armand, and Chin-Yin Tai for assistance with Western blotting; and W. Bryan Smith for help with Image J software. Confocal imaging was performed at the Caltech Biological Imaging Facility. This work was supported in part by NIH RO1 grant NS43416 to K.Z.; and by grants DA15495 and DA15383 to M.R. S.S. was supported in part by grant NIH T32 CA09213.

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