Host genome surveillance for retrotransposons by transposon-derived proteins

Cam, Hugh P.; Noma, Ken-ichi; Ebina, Hirotaka; Levin, Henry L.; Grewal, Shiv I. S.

doi:10.1038/nature06499

Cited by 159 publications

(254 citation statements)

References 53 publications

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“…Importantly, the localization of Mc at swi2 requires a CENP-B homolog, Abp1, the loss of which impairs Swi2 protein expression (this study) and RPC spreading (29). These results suggest that, in addition to silencing retrotransposons, CENP-B binding in different chromosomal contexts recruits factors important for other chromatin transactions, such as transcription (41). Abp1 bound to the swi2 promoter region facilitates preferential targeting of Mc, which normally binds an M-box sequence motif to activate M-specific genes by recruiting Ste11, a key transcription factor in the sexual differentiation pathway (24,30,42).…”

Section: Discussionmentioning

confidence: 54%

“…Another intriguing observation is that Mc localizes to sites of noncoding RNA production and several LTRs. Moreover, Mc binding at LTRs requires Abp1, which is also enriched at these loci (41). Further detailed investigation is needed to explore the significance of Mc localization at LTRs and ncRNA loci.…”

Section: Discussionmentioning

confidence: 99%

“…S8. swi2Δ, Swi2-myc, and abp1Δ have been described previously (18,41). Mutant swi6 strains used in this study contain the missense swi6-115 (W269R) allele that causes severe reduction in Swi6 protein levels (48).…”

Section: Methodsmentioning

confidence: 99%

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A homolog of male sex-determining factor SRY cooperates with a transposon-derived CENP-B protein to control sex-specific directed recombination

Matsuda

Sugioka-Sugiyama

Mizuguchi

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Schizosaccharomyces pombe cells switch mating type by replacing genetic information at the expressed mat1 locus with sequences copied from mat2-P or mat3-M silent donor loci. The choice of donor locus is dictated by cell type, such that mat2 is the preferred donor in M cells and mat3 is the preferred donor in P cells. Donor choice involves a recombination-promoting complex (RPC) containing Swi2 and Swi5. In P cells, the RPC localizes to a specific DNA element located adjacent to mat3, but in M cells it spreads across the silent mating-type region, including mat2-P. This differential distribution of the RPC regulates nonrandom choice of donors. However, celltype-specific differences in RPC localization are not understood. Here we show that the mat1-M-encoded factor Mc, which shares structural and functional similarities with the male sex-determining factor SRY, is highly enriched at the swi2 and swi5 loci and promotes elevated levels of RPC components. Loss of Mc reduces Swi2 and Swi5 to levels comparable to those in P cells and disrupts RPC spreading across the mat2/3 region. Mc also localizes to loci expressed preferentially in M cells and to retrotransposon LTRs. We demonstrate that Mc localization at LTRs and at swi2 requires Abp1, a homolog of transposon-derived CENP-B protein and that loss of Abp1 impairs Swi2 protein expression and the donor choice mechanism. These results suggest that Mc modulates levels of recombination factors, which is important for mating-type donor selection and for the biased gene conversion observed during meiosis, where M cells serve as preferential donors of genetic information. (1) and mating-type switching in the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe (2-5). In these distantly related yeast species, cells alternate between two distinct mating-type alleles by copying genetic information from one of the two silent donor loci to the active mating-type locus via highly orchestrated recombination processes (6-8).The mating-type region of S. pombe contains three linked locimat1, mat2, and mat3-located on chromosome 2. In wild-type homothallic strains, designated h 90 , mat2 is located ∼17 kb centromere-distal to mat1, whereas mat3 is separated from mat2 by an 11-kb interval ( Fig. 1) (8, 9). The mating type of a haploid cell is determined by the presence of P or M information at mat1 (8). Each allele consists of two divergently transcribed genes (10). mat1-P contains the Pc and Pi genes, and mat1-M contains the Mc and Mi genes. mat2 and mat3 contain the same genetic information as mat1-P and mat1-M, respectively, but are maintained in a silent state. These silent mating-type cassettes are embedded in a 20-kb heterochromatin domain surrounded by inverted repeat (IR-R and IR-

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Section: Discussionmentioning

confidence: 54%

Section: Discussionmentioning

confidence: 99%

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A homolog of male sex-determining factor SRY cooperates with a transposon-derived CENP-B protein to control sex-specific directed recombination

Matsuda

Sugioka-Sugiyama

Mizuguchi

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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“…To see whether Tf2 derepression is always associated with Rad52 binding to Tf2 cDNA, we carried out SPI-seq analysis on ams2D, as well as two other mutants defective in Tf2 silencing, the HIRA histone chaperone mutant slm9D and the CENP-B mutant cbp1D (Greenall et al 2006;Cam et al 2008). In both ams2D and slm9D, we observed Rad52 enrichment on Tf2, with patterns similar to those in D1D3 (Fig.…”

Section: Rad52 Enrichment Patterns In Pfh1 Helicase Mutantsmentioning

confidence: 74%

Mapping genomic hotspots of DNA damage by a single-strand-DNA-compatible and strand-specific ChIP-seq method

Zhou

Zhang

et al. 2012

Genome Res.

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Spontaneous DNA damage may occur nonrandomly in the genome, especially when genome maintenance mechanisms are undermined. We developed single-strand DNA (ssDNA)-associated protein immunoprecipitation followed by sequencing (SPI-seq) to map genomic hotspots of DNA damage. We demonstrated this method with Rad52, a homologous recombination repair protein, which binds to ssDNA formed at DNA lesions. SPI-seq faithfully detected, in fission yeast, Rad52 enrichment at artificially induced double-strand breaks (DSBs) as well as endogenously programmed DSBs for mating-type switching. Applying Rad52 SPI-seq to fission yeast mutants defective in DNA helicase Pfh1 or histone H3K56 deacetylase Hst4, led to global views of DNA lesion hotspots emerging in these mutants. We also found serendipitously that histone dosage aberration can activate retrotransposon Tf2 and cause the accumulation of a Tf2 cDNA species bound by Rad52. SPI-seq should be widely applicable for mapping sites of DNA damage and uncovering the causes of genome instability.

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“…In contrast, Tf2 mRNA expression increased in the class II histone deacetylase clr3Δ and the class I histone deacetylase clr6Δ mutants, suggesting RNAi-independent regulation of Tf2 chromatin structure. In the current study, Grewal and colleagues further investigated RNAi-independent mechanisms that regulate transposon activity [4].…”

mentioning

confidence: 98%