Acknowledgements We thank M. Kobayashi, D. Engel, M. Muramatsu and T. Honjo for
discussion and comments on the manuscript, M. Busslinger for information on RT–PCR analysis,
N. Kaneko for the preparation of tissue sections, and M. Kanno for the use of FACS machinery.
This work was supported by Grants-in-aid from the Ministry of Education, Culture, Sport,
Science and Technology of Japan and Hiroshima University 21st century COE programme. A.M.
was initially supported by the Research Fellowships for Young Scientists from the Japanese Society
for Promotion of Science.
Competing interests statement The authors declare that they have no competing financial
interests.
Correspondence and requests for materials should be addressed to K.I.
(igarak@hiroshima-u.ac.jp).
..............................................................
Intergenic transcription is required
to repress the Saccharomyces
cerevisiae SER3 gene
Joseph A. Martens, Lisa Laprade & Fred Winston
Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur,
Boston, Massachusetts 02115, USA
.............................................................................................................................................................................
Transcription by RNA polymerase II in Saccharomyces cerevisiae
and in humans is widespread, even in genomic regions that do
not encode proteins
1–6
. The purpose of such intergenic transcrip-
tion is largely unknown, although it can be regulatory
7,8
. We have
discovered a role for one case of intergenic transcription by
studying the S. cerevisiae SER3 gene. Our previous results
demonstrated that transcription of SER3 is tightly repressed
during growth in rich medium
9
. We now show that the regulatory
region of this gene is highly transcribed under these conditions
and produces a non-protein-coding RNA (SRG1). Expression of
the SRG1 RNA is required for repression of SER3. Additional
experiments have demonstrated that repression occurs by a
transcription-interference mechanism in which SRG1 transcrip-
tion across the SER3 promoter interferes with the binding of
activators. This work identifies a previously unknown class of
transcriptional regulatory genes.
The S. cerevisiae SER3 gene encodes a phosphoglycerate dehy-
drogenase that catalyses a step in serine biosynthesis
10
. To investi-
gate SER3 repression in greater detail, we performed chromatin
immunoprecipitation (ChIP) experiments to test for the association
of general transcription factors with the SER3 regulatory region
in vivo. Surprisingly, our results showed that under repressing
conditions, a significant level of both TATA-binding protein
(TBP) and RNA polymerase II (Pol II) bind 5
0
of the SER3 TATA
element (Fig. 1a). Additional ChIP experiments showed that other
factors, including phosphorylated forms of Pol II and mRNA
capping factors, are also associated with this region (unpublished
data). Thus, when SER3 is repressed, its regulatory region is
associated with factors required for active transcription. As
described below, this region contains a second TATA element
(shown in Fig. 1a).
To determine whether transcription occurs in the SER3 regula-
tory region, we performed transcription run-on experiments. These
results showed that there is a high level of active transcription
(Fig. 1b, probes 3–5). This transcription occurs on the same strand
as SER3 as determined by its hybridization specificity for single-
stranded probes.
We gained additional insight into the transcription occurring 5
0
of SER3 by comparing the DNA sequence of this region to that
of four yeasts closely related to S. cerevisiae
11,12
. This analysis
(Supplementary Fig. 1) revealed that, in addition to the TATA
element proximal to the SER3 coding region (2103 relative to the
SER3 ATG), there is a second TATA element at 2558 that is perfectly
conserved in all five yeasts. Short conserved sequences 5
0
of this
TATAelement suggest the presence of regulatory sites. Within the
transcribed region, there are three conserved sequence motifs
between 2262 and 2156. Deletion analysis strongly suggests that
this region functions as a SER3 upstream activating sequence (UAS)
(Supplementary Fig. 2). Outside of these sequence elements there
is no significant conservation or open reading frame in this
region, suggesting that it does not encode a protein. Because this
region is transcribed and, as will be shown, has an identified
function, we have designated it as the SRG1 gene (SER3 regulatory
gene 1). We will refer to the TATA element at 2558 as the SRG1
TATA element.
To test for a role for SRG1 in SER3 repression, we constructed a
mutation in the SRG1 TATA sequence, from TATAAA to CCTAGG
(srg1-1). By northern analysis, the SRG1 transcript in a wild-type
strain appears primarily as a diffuse band of approximately 550
bases (Fig. 2a). A longer RNA transcript is also present at a
lower level whose length is consistent with initiation at the SRG1
initiation site and readthrough across SER3. In the srg1-1 TATA
mutant, both RNAs are undetectable. Significantly, SER3 transcrip-
tion is derepressed to a high level in this mutant, demonstrating an
Figure 1 Evidence for active transcription 5
0
of SER3. a, ChIP analysis at SER3. ChIP
analysis of TBP and Pol II (Rpb3) was performed on wild-type strain FY2245 grown in
repressing conditions (YPD medium). A representative set of PCR reactions from two-fold
dilutions of chromatin is shown. The regions amplified by PCR (A–D) are marked by
blue bars in the diagram of the SER3 promoter on the right. The control primer set
amplifies a region of chromosome V that lacks open reading frames
25
. The graphs
summarize the results of three independent experiments, with each value representing
the average and standard error of the fold enrichment (ratio of the percentage of SER3
immunoprecipitated to the percentage of the control region immunoprecipitated).
b, Transcription run-on analysis at SER3. Transcription run-on analysis was performed on
wild-type strain FY2097 grown in repressing conditions. A schematic of SER3 is shown,
with the green bars representing antisense oligonucleotides that detect transcription from
the Watson strand. The two yellow bars (N4, N5) represent sense oligonucleotides used as
negative controls. An oligonucleotide that detects transcription of ACT1 was included as a
positive control.
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