NAP-I is a functional homologue of TAF-I that is required for replication and transcription of the adenovirus genome in a chromatin-like structure

Hiroyuki Kawase, Mitsuru Okuwaki, Mary Miyaji, Reiko Ohba, Hiroshi Handa, Yukio Ishimi, Tomoko Fujii-Nakata, Akihiko Kikuchi, Kyosuke Nagata

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

Background: For the activation of replication and transcription from DNA in a chromatin structure, a variety of factors are thought to be needed that alter the chromatin structure. Template activating factor-I (TAF-I) has been identified as such a host factor required for replication of the adenovirus (Ad) genome complexed with viral basic core proteins (Ad core). TAF-I also stimulates transcription from the Ad core DNA. Results: Using mutant TAF-I proteins, we have demonstrated that the acidic stretch present in the carboxyl terminal region is essential for the stimulation of transcription from the Ad core. A genomic footprinting experiment with restriction endonuclease has revealed that TAF-I causes a structural change in the Ad core. TAF-I has been shown to have significant amino acid similarity to nucleosome assembly protein-I (NAP-I), which is involved in the formation of the chromatin structure. We have shown that TAF-I can be substituted by NAP-I in the activation of the cell-free Ad core transcription system. Two of the tripartite acidic regions and the region homologous to TAF-I in NAP-I are required for the maximal TAF-I activity of NAP-I. Furthermore, TAF-I has been shown to have NAP-I activity, and the acidic region of TAF-I is required for this activity. Conclusions: Since TAF-I causes the structural change of the Ad core and thereby activates transcription, TAF-I is thought to be one of the proteins which is involved in chromatin remodeling. NAP-I is structurally related to TAF-I and functionally substitutes for TAF-I. Furthermore, TAF-I has NAP-I activity. These observations suggest that this type of molecule has dual functions, possibly by participating in facilitating the assembly of the chromatin structure as well as perturbing the chromatin structure to allow transcription to proceed.

Original languageEnglish
Pages (from-to)1045-1056
Number of pages12
JournalGenes to Cells
Volume1
Issue number12
Publication statusPublished - 1996
Externally publishedYes

Fingerprint

Nucleosomes
Adenoviridae
Chromatin
Genome
Proteins
Chromatin Assembly and Disassembly
Viral Core Proteins
DNA Restriction Enzymes
DNA Replication
Transcriptional Activation
Amino Acids
DNA

ASJC Scopus subject areas

  • Cell Biology
  • Genetics

Cite this

NAP-I is a functional homologue of TAF-I that is required for replication and transcription of the adenovirus genome in a chromatin-like structure. / Kawase, Hiroyuki; Okuwaki, Mitsuru; Miyaji, Mary; Ohba, Reiko; Handa, Hiroshi; Ishimi, Yukio; Fujii-Nakata, Tomoko; Kikuchi, Akihiko; Nagata, Kyosuke.

In: Genes to Cells, Vol. 1, No. 12, 1996, p. 1045-1056.

Research output: Contribution to journalArticle

Kawase, H, Okuwaki, M, Miyaji, M, Ohba, R, Handa, H, Ishimi, Y, Fujii-Nakata, T, Kikuchi, A & Nagata, K 1996, 'NAP-I is a functional homologue of TAF-I that is required for replication and transcription of the adenovirus genome in a chromatin-like structure', Genes to Cells, vol. 1, no. 12, pp. 1045-1056.
Kawase, Hiroyuki ; Okuwaki, Mitsuru ; Miyaji, Mary ; Ohba, Reiko ; Handa, Hiroshi ; Ishimi, Yukio ; Fujii-Nakata, Tomoko ; Kikuchi, Akihiko ; Nagata, Kyosuke. / NAP-I is a functional homologue of TAF-I that is required for replication and transcription of the adenovirus genome in a chromatin-like structure. In: Genes to Cells. 1996 ; Vol. 1, No. 12. pp. 1045-1056.
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abstract = "Background: For the activation of replication and transcription from DNA in a chromatin structure, a variety of factors are thought to be needed that alter the chromatin structure. Template activating factor-I (TAF-I) has been identified as such a host factor required for replication of the adenovirus (Ad) genome complexed with viral basic core proteins (Ad core). TAF-I also stimulates transcription from the Ad core DNA. Results: Using mutant TAF-I proteins, we have demonstrated that the acidic stretch present in the carboxyl terminal region is essential for the stimulation of transcription from the Ad core. A genomic footprinting experiment with restriction endonuclease has revealed that TAF-I causes a structural change in the Ad core. TAF-I has been shown to have significant amino acid similarity to nucleosome assembly protein-I (NAP-I), which is involved in the formation of the chromatin structure. We have shown that TAF-I can be substituted by NAP-I in the activation of the cell-free Ad core transcription system. Two of the tripartite acidic regions and the region homologous to TAF-I in NAP-I are required for the maximal TAF-I activity of NAP-I. Furthermore, TAF-I has been shown to have NAP-I activity, and the acidic region of TAF-I is required for this activity. Conclusions: Since TAF-I causes the structural change of the Ad core and thereby activates transcription, TAF-I is thought to be one of the proteins which is involved in chromatin remodeling. NAP-I is structurally related to TAF-I and functionally substitutes for TAF-I. Furthermore, TAF-I has NAP-I activity. These observations suggest that this type of molecule has dual functions, possibly by participating in facilitating the assembly of the chromatin structure as well as perturbing the chromatin structure to allow transcription to proceed.",
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T1 - NAP-I is a functional homologue of TAF-I that is required for replication and transcription of the adenovirus genome in a chromatin-like structure

AU - Kawase, Hiroyuki

AU - Okuwaki, Mitsuru

AU - Miyaji, Mary

AU - Ohba, Reiko

AU - Handa, Hiroshi

AU - Ishimi, Yukio

AU - Fujii-Nakata, Tomoko

AU - Kikuchi, Akihiko

AU - Nagata, Kyosuke

PY - 1996

Y1 - 1996

N2 - Background: For the activation of replication and transcription from DNA in a chromatin structure, a variety of factors are thought to be needed that alter the chromatin structure. Template activating factor-I (TAF-I) has been identified as such a host factor required for replication of the adenovirus (Ad) genome complexed with viral basic core proteins (Ad core). TAF-I also stimulates transcription from the Ad core DNA. Results: Using mutant TAF-I proteins, we have demonstrated that the acidic stretch present in the carboxyl terminal region is essential for the stimulation of transcription from the Ad core. A genomic footprinting experiment with restriction endonuclease has revealed that TAF-I causes a structural change in the Ad core. TAF-I has been shown to have significant amino acid similarity to nucleosome assembly protein-I (NAP-I), which is involved in the formation of the chromatin structure. We have shown that TAF-I can be substituted by NAP-I in the activation of the cell-free Ad core transcription system. Two of the tripartite acidic regions and the region homologous to TAF-I in NAP-I are required for the maximal TAF-I activity of NAP-I. Furthermore, TAF-I has been shown to have NAP-I activity, and the acidic region of TAF-I is required for this activity. Conclusions: Since TAF-I causes the structural change of the Ad core and thereby activates transcription, TAF-I is thought to be one of the proteins which is involved in chromatin remodeling. NAP-I is structurally related to TAF-I and functionally substitutes for TAF-I. Furthermore, TAF-I has NAP-I activity. These observations suggest that this type of molecule has dual functions, possibly by participating in facilitating the assembly of the chromatin structure as well as perturbing the chromatin structure to allow transcription to proceed.

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