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SREBP controls oxygen-dependent mobilization of retrotransposons in fission yeast.

Sehgal A, Lee CY, Espenshade PJ - PLoS Genet. (2007)

Bottom Line: Transposons do not encode transcription factors and thus rely on host factors for mRNA expression and survival.Sre1 binds to DNA sequences in the Tf2 long terminal repeat that functions as an oxygen-dependent promoter.We find that Tf2 solo long terminal repeats throughout the genome direct oxygen-dependent expression of adjacent coding and noncoding sequences, providing a potential mechanism for the generation of oxygen-dependent gene expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland, Unites States of America.

ABSTRACT
Retrotransposons are mobile genetic elements that proliferate through an RNA intermediate. Transposons do not encode transcription factors and thus rely on host factors for mRNA expression and survival. Despite information regarding conditions under which elements are upregulated, much remains to be learned about the regulatory mechanisms or factors controlling retrotransposon expression. Here, we report that low oxygen activates the fission yeast Tf2 family of retrotransposons. Sre1, the yeast ortholog of the mammalian membrane-bound transcription factor sterol regulatory element binding protein (SREBP), directly induces the expression and mobilization of Tf2 retrotransposons under low oxygen. Sre1 binds to DNA sequences in the Tf2 long terminal repeat that functions as an oxygen-dependent promoter. We find that Tf2 solo long terminal repeats throughout the genome direct oxygen-dependent expression of adjacent coding and noncoding sequences, providing a potential mechanism for the generation of oxygen-dependent gene expression.

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Low Oxygen Stimulates Sre1-Dependent, Tf2 Mobilization(A) Tf2–12-neoAI yeast cells were grown in the absence of oxygen for 8 h to induce transcription, cDNA synthesis, and mobilization. Cells were assayed for acquisition of G418-resistance as described in Materials and Methods. Frequency of G418-resistance for different strains is shown.(B) Genomic DNA was isolated from the parent Tf2–12-neoAI strain (lane 1) and nine G418-resistant progeny strains (lanes 2–10), digested with HindIII, and analyzed by Southern blotting using a neo probe. neoAI denotes the neo gene with the artificial intron present in the Tf2–12-neoAI parent strain.
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pgen-0030131-g004: Low Oxygen Stimulates Sre1-Dependent, Tf2 Mobilization(A) Tf2–12-neoAI yeast cells were grown in the absence of oxygen for 8 h to induce transcription, cDNA synthesis, and mobilization. Cells were assayed for acquisition of G418-resistance as described in Materials and Methods. Frequency of G418-resistance for different strains is shown.(B) Genomic DNA was isolated from the parent Tf2–12-neoAI strain (lane 1) and nine G418-resistant progeny strains (lanes 2–10), digested with HindIII, and analyzed by Southern blotting using a neo probe. neoAI denotes the neo gene with the artificial intron present in the Tf2–12-neoAI parent strain.

Mentions: To measure transposition, we cultured Tf2–12-neoAI cells in the presence or absence of oxygen for 8 h and then plated cells on selective medium containing G418 to determine the frequency of transposition. The basal aerobic frequency of Tf2–12-neoAI transposition (2.5 × 10−8/cell) increased 18-fold (44 × 10−8/cell) under low oxygen (Figure 4A). As expected, this oxygen-dependent increase in transposition frequency required Sre1. First, cells lacking sre1+ showed no increase in transposition under low oxygen. Second, deletion of the Sre1 DNA binding sequence from the Tf2 5′ LTR resulted in the loss of oxygen-dependent induction of transposition (Tf2 ΔSRE, Figure 4A). Importantly, this assay monitored only one of the 12 oxygen-responsive Tf2 elements in the fission yeast genome [30]. Thus, we expect the actual transposition frequency under low oxygen to be >10-fold higher (∼5 × 10−6/cell).


SREBP controls oxygen-dependent mobilization of retrotransposons in fission yeast.

Sehgal A, Lee CY, Espenshade PJ - PLoS Genet. (2007)

Low Oxygen Stimulates Sre1-Dependent, Tf2 Mobilization(A) Tf2–12-neoAI yeast cells were grown in the absence of oxygen for 8 h to induce transcription, cDNA synthesis, and mobilization. Cells were assayed for acquisition of G418-resistance as described in Materials and Methods. Frequency of G418-resistance for different strains is shown.(B) Genomic DNA was isolated from the parent Tf2–12-neoAI strain (lane 1) and nine G418-resistant progeny strains (lanes 2–10), digested with HindIII, and analyzed by Southern blotting using a neo probe. neoAI denotes the neo gene with the artificial intron present in the Tf2–12-neoAI parent strain.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC1941750&req=5

pgen-0030131-g004: Low Oxygen Stimulates Sre1-Dependent, Tf2 Mobilization(A) Tf2–12-neoAI yeast cells were grown in the absence of oxygen for 8 h to induce transcription, cDNA synthesis, and mobilization. Cells were assayed for acquisition of G418-resistance as described in Materials and Methods. Frequency of G418-resistance for different strains is shown.(B) Genomic DNA was isolated from the parent Tf2–12-neoAI strain (lane 1) and nine G418-resistant progeny strains (lanes 2–10), digested with HindIII, and analyzed by Southern blotting using a neo probe. neoAI denotes the neo gene with the artificial intron present in the Tf2–12-neoAI parent strain.
Mentions: To measure transposition, we cultured Tf2–12-neoAI cells in the presence or absence of oxygen for 8 h and then plated cells on selective medium containing G418 to determine the frequency of transposition. The basal aerobic frequency of Tf2–12-neoAI transposition (2.5 × 10−8/cell) increased 18-fold (44 × 10−8/cell) under low oxygen (Figure 4A). As expected, this oxygen-dependent increase in transposition frequency required Sre1. First, cells lacking sre1+ showed no increase in transposition under low oxygen. Second, deletion of the Sre1 DNA binding sequence from the Tf2 5′ LTR resulted in the loss of oxygen-dependent induction of transposition (Tf2 ΔSRE, Figure 4A). Importantly, this assay monitored only one of the 12 oxygen-responsive Tf2 elements in the fission yeast genome [30]. Thus, we expect the actual transposition frequency under low oxygen to be >10-fold higher (∼5 × 10−6/cell).

Bottom Line: Transposons do not encode transcription factors and thus rely on host factors for mRNA expression and survival.Sre1 binds to DNA sequences in the Tf2 long terminal repeat that functions as an oxygen-dependent promoter.We find that Tf2 solo long terminal repeats throughout the genome direct oxygen-dependent expression of adjacent coding and noncoding sequences, providing a potential mechanism for the generation of oxygen-dependent gene expression.

View Article: PubMed Central - PubMed

Affiliation: Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland, Unites States of America.

ABSTRACT
Retrotransposons are mobile genetic elements that proliferate through an RNA intermediate. Transposons do not encode transcription factors and thus rely on host factors for mRNA expression and survival. Despite information regarding conditions under which elements are upregulated, much remains to be learned about the regulatory mechanisms or factors controlling retrotransposon expression. Here, we report that low oxygen activates the fission yeast Tf2 family of retrotransposons. Sre1, the yeast ortholog of the mammalian membrane-bound transcription factor sterol regulatory element binding protein (SREBP), directly induces the expression and mobilization of Tf2 retrotransposons under low oxygen. Sre1 binds to DNA sequences in the Tf2 long terminal repeat that functions as an oxygen-dependent promoter. We find that Tf2 solo long terminal repeats throughout the genome direct oxygen-dependent expression of adjacent coding and noncoding sequences, providing a potential mechanism for the generation of oxygen-dependent gene expression.

Show MeSH
Related in: MedlinePlus