© 2005 Nature Publishing Group
The yeast Pif1p helicase removes
telomerase from telomeric DNA
Jean-Baptiste Boule ´
1
*, Leticia R. Vega
1
*† & Virginia A. Zakian
1
Telomeres are the physical ends of eukaryotic chromosomes. Genetic studies have established that the baker’s yeast
Pif1p DNA helicase is a negative regulator of telomerase, the specialized reverse transcriptase that maintains telomeric
DNA, but the biochemical basis for this inhibition was unknown. Here we show that in vitro, Pif1p reduces the
processivity of telomerase and releases telomerase from telomeric oligonucleotides. The released telomerase is
enzymatically active because it is able to lengthen a challenger oligonucleotide. In vivo, overexpression of Pif1p reduces
telomerase association with telomeres, whereas depleting cells of Pif1p increases the levels of telomere-bound Est1p, a
telomerase subunit that is present on the telomere when telomerase is active. We propose that Pif1p helicase activity
limits telomerase action both in vivo and in vitro by displacing active telomerase from DNA ends.
Saccharomyces cerevisiae telomeres consist of ,350 base pairs of the
sequence C
1–3
A/TG
1–3
. As in most eukaryotes, yeast telomeric DNA
is elongated by telomerase, a specialized reverse transcriptase. Yeast
telomerase contains the catalytic subunit (Est2p), the templating
RNA (TLC1) and additional protein subunits, such as Est1p, that
participate in the recruitment or activation of the enzyme.
From yeasts to humans, telomerase activity is highly regulated.
Yeast telomerase can lengthen telomeres only in late S/G2 phase
1,2
,
even though the catalytic core of telomerase is telomere-bound
throughout most of the cell cycle
3,4
. In contrast, Est1p is telomere-
associated only in late S/G2 phase, the time of telomerase action
3–5
.
Pif1p is a 5
0
to 3
0
helicase that inhibits telomerase-mediated
telomere lengthening
6,7
and de novo telomere addition
6,8,9
. In the
absence of Pif1p, telomeres increase in length by ,100 base pairs,
whereas Pif1p overexpression results in an ,80-base-pair decrease in
telomere length
6,7
. Lack of Pif1p results in a ,600-fold increase in de
novo telomere addition at spontaneous double-strand breaks
6
, and a
,1,000-fold increase in the generation of the types of gross chro-
mosomal rearrangements that occur during tumour formation by
addition of telomeric DNA to spontaneous chromosome breaks
9
.
Cells expressing the catalytically-inactive Pif1p
K264A
have the same
phenotype as pif1D cells, and cells overexpressing Pif1p
K264A
do not
exhibit telomere shortening. Thus, the catalytic activity of Pif1p is
required for its effects on telomeres. As Pif1p is telomere-associated
in vivo, it probably affects telomerase directly
7
.
There is increasing evidence that positive and negative regulation
of telomerase contributes to genome integrity. Here we employ in
vitro and in vivo assays to show that Pif1p acts catalytically to remove
telomerase from telomeric DNA.
Specificity of Pif1p helicase activity
We purified the nuclear forms of both wild-type Pif1p and the
helicase-inactive Pif1p
K264A
(ref. 7) (Fig. 1a) and tested their ability
to unwind 20-base oligonucleotide DNA/DNA, RNA/RNA or RNA/
DNA duplexes of identical nucleotide sequence, except that U
replaced T in the RNA strands (Fig. 1b; see Methods for sequence
of the helicase substrate). All substrates contained the same 20
nucleotide single-stranded 5
0
overhang, which is required for Pif1p
unwinding
10
. As expected, recombinant Pif1p unwound the DNA/
DNA substrate (Fig. 1b, lane 2). Pif1p also unwound the RNA/DNA
hybrid in which the strand containing the single-stranded 5
0
over-
hang was made of DNA (Fig. 1b, lane 4) but not when it was made of
RNA (Fig. 1b, lane 6), nor did it unwind an RNA duplex (Fig. 1b,
lane 8). As assessed by bandshift experiments, Pif1p bound to single-
stranded DNA but not significantly to single-stranded RNA (data not
shown). Therefore, Pif1p requires a deoxyribose backbone to load
onto its substrate. As expected, Pif1p
K264A
had no unwinding activity
(Fig. 1b, lanes 9–12), although it bound efficiently to single-stranded
DNA (see Supplementary Fig. S2).
Pif1p reduces telomerase processivity
Processivity describes an enzyme’s ability to undergo multiple reac-
tion cycles without being released from its substrate. Two types of
processivity have been defined for telomerase, nucleotide addition
processivity and repeat addition processivity
11
. The first refers to the
ability of telomerase to copy the entire template region of the RNA
Figure 1 | Activity of Pif1p. a, Purified wild-type Pif1p and Pif1p
K264A
were
analysed by Coomassie staining (left) or western blotting (right).
b, Radiolabelled substrates were incubated with 60 nM Pif1p (left) or
Pif1p
K264A
(right). At 0 and 15 min after ATP addition, aliquots were
withdrawn and examined by electrophoresis. RNA strands are represented
with open rectangles and DNA strands are represented by filled rectangles.
1
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. †Present address: Barry University, School of Natural and Health Sciences, Miami
Shores, Florida 33161, USA.
*These authors contributed equally to this work.
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