A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Xylourgidis, N., Roth, P., Sabri, N., Tsarouhas, V., Samakovlis, C. (2006). The nucleoporin Nup214 sequesters CRM1 at the nuclear rim and modulates NFkappaB activation in Drosophila.  J. Cell Sci. 119(Pt 21): 4409--4419. (Export to RIS)
FlyBase ID FBrf0191995
Publication Type Research paper
PubMed ID 17032737
PubMed Abstract CRM1-mediated protein export is an important determinant of the nuclear accumulation of many gene regulators. Here, we show that the NFkappaB transcription factor Dorsal is a substrate of CRM1 and requires the nucleoporin Nup214 for its nuclear translocation upon signaling. Nup214 bound to CRM1 directly and anchored it to the nuclear envelope. In nup214 mutants CRM1 accumulated in the nucleus and NES-protein export was enhanced. Nup214 formed complexes with Nup88 and CRM1 in vivo and Nup214 protected Nup88 from degradation at the nuclear rim. In turn, Nup88 was sufficient for targeting the complex to the nuclear pores. Overexpression experiments indicated that Nup214 alone attracts a fraction of CRM1 to the nuclear envelope but does not interfere with NES-GFP export. By contrast, overexpression of the Nup214-Nup88 complex trapped CRM1 and Dorsal to cytoplasmic foci and inhibited protein export and immune response activation. We hypothesize that variation in levels of the Nup214-Nup88 complex at the pore changes the amount of NPC-bound CRM1 and influences the relative strength and duration of NFkappaB signaling responses.
DOI 10.1242/jcs.03201
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Language of Publication English
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Publication Type Journal
Abbreviation J. Cell Sci.
Title Journal of Cell Science
Publication Year 1966-
ISBN/ISSN 0021-9533
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