It's been known for quite a while that ADH1 transcription is NOT constitutive
but regulated according to carbon source. This was first reported by Denis et
al. (JBC 258:1165-1171 [1983]), and was confirmed by us in an analysis of the
contribution of RAP1 and GCR1 to ADH1 promoter function (RAP1/GCR1
interdependent activation accounts for most of ADH1 mRNA production in cells
grown either on a fermentable or a nonfermentable carbon source; see Gene
90:79-85 [1990] and MCB 10:859-862 [1990]). We have fused the ADH1 promoter to
a heterologous reporter gene, which results in approximately 5-fold higher
activation in glucose-grown cells than in pyruvate- or ethanol-grown cells,
indicating that it is the ADH1 promoter per se that confers carbon source
regulation (unpublished data). Our unpublished results also indicate that ADH1
transcription initiation is regulated according to growth phase, such that the
highest levels occur in early log and a five-fold down effect is seen by
stationary phase. Steve Kron has recently suggested that it makes sense for
ADH1 levels to be high in the presence of accumulated ethanol. He must be
referring to ADH enzyme activity, not expression of the ADH1 gene, since it is
a different ADH-encoding gene, ADH2, that is transcriptionally derepressed and
responsible for the extremely high levels of ADH in cells grown on ethanol or
after diauxic shift in rich media. ADH2 expression is negligible in
glucose-grown cells.
George Santangelo
Joanne Tornow
University of Southern Mississippi
santnglo at whale.st.usm.edujtornow at whale.st.usm.edu
