Yeast sec mutations define the machinery of vesicular traffic. Surprisingly
, many of these mutations also inhibit ribosome biogenesis by reducing tran
scription of rRNA and genes encoding ribosomal proteins. We observe that th
ese mutants reversibly inhibit protein import into the nucleus, with import
cargo accumulating at the nucleoplasmic face of nuclear pore complexes, as
when Ran-GTP cannot bind importins. They also rapidly and reversibly reloc
ate multiple nucleolar and nucleoplasmic proteins to the cytoplasm. The imp
ort block and relocation are antagonized by overexpression of yeast Ran, Ho
g1p kinase, or Ssa/Hsp70 proteins or by inhibition of protein synthesis. Th
ese nucleocytoplasmic signaling events document an extraordinary plasticity
of nuclear organization.