Key result
Loss of function mutations in Drosophila Profilin (chic) and gain of function mutations in Sd (RanGAP) suppress the severe eye phenotype caused by reduction of NTF2, indicating that Profilin and actin cytoskeleton organization play an important role in nuclear trafficking.
Profilin and the organization of the actin cytoskeleton play an important role in Ran-mediated nuclear trafficking in a Drosophila model.
Links actin cytoskeleton to nuclear transport in Drosophila; hypothesis-generating and leaves open mammalian relevance.
BACKGROUND: Transport of macromolecules into and out of the nucleus is a highly regulated process. The RanGTP/RanGDP gradient controls the trafficking of molecules exceeding the diffusion limit of the nuclear pore across the nuclear envelope. RESULTS: We found genetic interaction between genes establishing the Ran gradient, nuclear transport factor 2 (ntf-2), Ran GTPase activating protein (Sd), and the gene encoding Drosophila Profilin, chickadee (chic). The severe eye phenotype caused by reduction of NTF2 is suppressed by loss of function mutations in chic and gain of function mutations in Sd (RanGAP). We show that in chic mutants, as in Sd-RanGAP, nuclear export is impaired. CONCLUSION: Our data suggest that Profilin and the organization of the actin cytoskeleton play an important role in nuclear trafficking.
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Minakhina et al. (2005) studied ntf-2 mutation eye phenotype. Loss of function mutations in Profilin (chic) and gain of function mutations in Sd (RanGAP) vs. Wild-type was evaluated on Suppression of ntf-2 eye phenotype and nuclear export impairment. Loss of function mutations in Drosophila Profilin (chic) and gain of function mutations in Sd (RanGAP) suppress the severe eye phenotype caused by reduction of NTF2, indicating that Profilin and actin cytoskeleton organization play an important role in nuclear trafficking.
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