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Vol. 11, Issue 6, 2103-2115, June 2000
Department of Molecular Biology, University of Texas Southwestern
Medical Center, Dallas, Texas 75390-9148
Cells modulate the expression of nuclear genes in response to
changes in the functional state of mitochondria, an interorganelle communication pathway called retrograde regulation. In yeast, expression of the CIT2 gene shows a typical retrograde
response in that its expression is dramatically increased in cells with dysfunctional mitochondria, such as in 
o petites. Three
genes control this signaling pathway: RTG1 and RTG3, which encode basic helix-loop-helix leucine zipper
transcription factors that bind as heterodimer to the
CIT2 upstream activation site, and RTG2,
which encodes a protein of unknown function. We show that in
respiratory-competent (+) cells in which
CIT2 expression is low, Rtg1p and Rtg3p exist as a
complex largely in the cytoplasm, and in o petites in
which CIT2 expression is high, they exist as a complex predominantly localized in the nucleus. Cytoplasmic Rtg3p is multiply phosphorylated and becomes partially dephosphorylated when localized in
the nucleus. Rtg2p, which is cytoplasmic in both + and
o cells, is required for the dephosphorylation and
nuclear localization of Rtg3p. Interaction of Rtg3p with Rtg1p is
required to retain Rtg3p in the cytoplasm of + cells; in
the absence of such interaction, nuclear localization and
dephosphorylation of Rtg3p is independent of Rtg2p. Our data show that
Rtg1p acts as both a positive and negative regulator of the retrograde
response and that Rtg2p acts to transduce mitochondrial signals
affecting the phosphorylation state and subcellular localization of Rtg3p.
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