Heterochromatin suppresses gross chromosomal rearrangements at centromeres by repressing Tfs1/TFIIS-dependent transcription

Akiko K Okita, Faria Zafar, Jie Su, Dayalini Weerasekara, Takuya Kajitani, Tatsuro S Takahashi, Hiroshi Kimura, Yota Murakami, Hisao Masukata, Takuro Nakagawa

研究成果: ジャーナルへの寄稿記事

抄録

Heterochromatin, characterized by histone H3 lysine 9 (H3K9) methylation, assembles on repetitive regions including centromeres. Although centromeric heterochromatin is important for correct segregation of chromosomes, its exact role in maintaining centromere integrity remains elusive. Here, we found in fission yeast that heterochromatin suppresses gross chromosomal rearrangements (GCRs) at centromeres. Mutations in Clr4/Suv39 methyltransferase increased the formation of isochromosomes, whose breakpoints were located in centromere repeats. H3K9A and H3K9R mutations also increased GCRs, suggesting that Clr4 suppresses centromeric GCRs via H3K9 methylation. HP1 homologs Swi6 and Chp2 and the RNAi component Chp1 were the chromodomain proteins essential for full suppression of GCRs. Remarkably, mutations in RNA polymerase II (RNAPII) or Tfs1/TFIIS, the transcription factor that facilitates restart of RNAPII after backtracking, specifically bypassed the requirement of Clr4 for suppressing GCRs. These results demonstrate that heterochromatin suppresses GCRs by repressing Tfs1-dependent transcription of centromere repeats.

元の言語英語
ページ(範囲)17
ジャーナルCommunications biology
2
DOI
出版物ステータス出版済み - 2019

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Heterochromatin
Centromere
RNA Polymerase II
Methylation
Mutation
Isochromosomes
Chromosome Segregation
Schizosaccharomyces
Nucleic Acid Repetitive Sequences
Methyltransferases
RNA Interference
Histones
Lysine
Transcription Factors
transcription factor S-II
Proteins

これを引用

Heterochromatin suppresses gross chromosomal rearrangements at centromeres by repressing Tfs1/TFIIS-dependent transcription. / Okita, Akiko K; Zafar, Faria; Su, Jie; Weerasekara, Dayalini; Kajitani, Takuya; Takahashi, Tatsuro S; Kimura, Hiroshi; Murakami, Yota; Masukata, Hisao; Nakagawa, Takuro.

:: Communications biology, 巻 2, 2019, p. 17.

研究成果: ジャーナルへの寄稿記事

Okita, AK, Zafar, F, Su, J, Weerasekara, D, Kajitani, T, Takahashi, TS, Kimura, H, Murakami, Y, Masukata, H & Nakagawa, T 2019, 'Heterochromatin suppresses gross chromosomal rearrangements at centromeres by repressing Tfs1/TFIIS-dependent transcription', Communications biology, 巻. 2, pp. 17. https://doi.org/10.1038/s42003-018-0251-z
Okita, Akiko K ; Zafar, Faria ; Su, Jie ; Weerasekara, Dayalini ; Kajitani, Takuya ; Takahashi, Tatsuro S ; Kimura, Hiroshi ; Murakami, Yota ; Masukata, Hisao ; Nakagawa, Takuro. / Heterochromatin suppresses gross chromosomal rearrangements at centromeres by repressing Tfs1/TFIIS-dependent transcription. :: Communications biology. 2019 ; 巻 2. pp. 17.
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abstract = "Heterochromatin, characterized by histone H3 lysine 9 (H3K9) methylation, assembles on repetitive regions including centromeres. Although centromeric heterochromatin is important for correct segregation of chromosomes, its exact role in maintaining centromere integrity remains elusive. Here, we found in fission yeast that heterochromatin suppresses gross chromosomal rearrangements (GCRs) at centromeres. Mutations in Clr4/Suv39 methyltransferase increased the formation of isochromosomes, whose breakpoints were located in centromere repeats. H3K9A and H3K9R mutations also increased GCRs, suggesting that Clr4 suppresses centromeric GCRs via H3K9 methylation. HP1 homologs Swi6 and Chp2 and the RNAi component Chp1 were the chromodomain proteins essential for full suppression of GCRs. Remarkably, mutations in RNA polymerase II (RNAPII) or Tfs1/TFIIS, the transcription factor that facilitates restart of RNAPII after backtracking, specifically bypassed the requirement of Clr4 for suppressing GCRs. These results demonstrate that heterochromatin suppresses GCRs by repressing Tfs1-dependent transcription of centromere repeats.",
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AU - Okita, Akiko K

AU - Zafar, Faria

AU - Su, Jie

AU - Weerasekara, Dayalini

AU - Kajitani, Takuya

AU - Takahashi, Tatsuro S

AU - Kimura, Hiroshi

AU - Murakami, Yota

AU - Masukata, Hisao

AU - Nakagawa, Takuro

PY - 2019

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N2 - Heterochromatin, characterized by histone H3 lysine 9 (H3K9) methylation, assembles on repetitive regions including centromeres. Although centromeric heterochromatin is important for correct segregation of chromosomes, its exact role in maintaining centromere integrity remains elusive. Here, we found in fission yeast that heterochromatin suppresses gross chromosomal rearrangements (GCRs) at centromeres. Mutations in Clr4/Suv39 methyltransferase increased the formation of isochromosomes, whose breakpoints were located in centromere repeats. H3K9A and H3K9R mutations also increased GCRs, suggesting that Clr4 suppresses centromeric GCRs via H3K9 methylation. HP1 homologs Swi6 and Chp2 and the RNAi component Chp1 were the chromodomain proteins essential for full suppression of GCRs. Remarkably, mutations in RNA polymerase II (RNAPII) or Tfs1/TFIIS, the transcription factor that facilitates restart of RNAPII after backtracking, specifically bypassed the requirement of Clr4 for suppressing GCRs. These results demonstrate that heterochromatin suppresses GCRs by repressing Tfs1-dependent transcription of centromere repeats.

AB - Heterochromatin, characterized by histone H3 lysine 9 (H3K9) methylation, assembles on repetitive regions including centromeres. Although centromeric heterochromatin is important for correct segregation of chromosomes, its exact role in maintaining centromere integrity remains elusive. Here, we found in fission yeast that heterochromatin suppresses gross chromosomal rearrangements (GCRs) at centromeres. Mutations in Clr4/Suv39 methyltransferase increased the formation of isochromosomes, whose breakpoints were located in centromere repeats. H3K9A and H3K9R mutations also increased GCRs, suggesting that Clr4 suppresses centromeric GCRs via H3K9 methylation. HP1 homologs Swi6 and Chp2 and the RNAi component Chp1 were the chromodomain proteins essential for full suppression of GCRs. Remarkably, mutations in RNA polymerase II (RNAPII) or Tfs1/TFIIS, the transcription factor that facilitates restart of RNAPII after backtracking, specifically bypassed the requirement of Clr4 for suppressing GCRs. These results demonstrate that heterochromatin suppresses GCRs by repressing Tfs1-dependent transcription of centromere repeats.

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DO - 10.1038/s42003-018-0251-z

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JO - Communications biology

JF - Communications biology

SN - 2399-3642

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