Genomic sequence, structural organization, molecular evolution, and aberrant rearrangement of promyelocytic leukemia zinc finger gene

T. Zhang, H. Xiong, L. X. Kan, C. K. Zhang, X. F. Jiao, G. Fu, Q. H. Zhang, L. Lu, J. H. Tong, B. W. Gu, M. Yu, J. X. Liu, J. Licht, S. Waxman, Arthur Z Zelent, E. Chen, S. J. Chen

Research output: Contribution to journalArticle

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Abstract

The promyelocytic leukemia zinc finger gene (PLZF) is involved in chromosomal translocation t(11;17) associated with acute promyelocytic leukemia. In this work, a 201-kilobase genomic DNA region containing the entire PLZF gene was sequenced. Repeated elements account for 19.83%, and no obvious coding information other than PLZF is present over this region. PLZF contains six exons and five introns, and the exon organization corresponds well with protein domains. There are at least four alternative splicings (AS- I, -II, -III, and -IV) within exon 1. AS-I could be detected in most tissues tested whereas AS-II, -III, and -IV were present in the stomach, testis, and heart, respectively. Although splicing donor and acceptor signals at exon- intron boundaries for AS-I and exons 1-6 were classical (gt-ag), AS-II, -III, and -IV had atypical splicing sites. These alternative splicings, nevertheless, maintained the ORF and may encode isoforms with absence of important functional domains. In mRNA species without AS-I, there is a relatively long 5' UTR of 6.0 kilobases. A TATA box and several transcription factor binding sites were found in the putative promoter region upstream of the transcription start site. PLZF is a well conserved gene from Caenorhabditis elegans to human. PLZF paralogous sequences are found in human genome. The presence of two MLL/PLZF-like alignments on human chromosome 11q23 and 19 suggests a syntenic replication during evolution. The chromosomal breakpoints and joining sites in the index acute promyelocytic leukemia case with t(11;17) also were characterized, which suggests the involvement of DNA damage-repair mechanism.

Original languageEnglish (US)
Pages (from-to)11422-11427
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume96
Issue number20
DOIs
StatePublished - Sep 28 1999
Externally publishedYes

Fingerprint

Molecular Evolution
Zinc Fingers
Leukemia
Exons
Genes
Acute Promyelocytic Leukemia
Alternative Splicing
Introns
Chromosomes, Human, Pair 19
Genetic Translocation
TATA Box
5' Untranslated Regions
Transcription Initiation Site
Caenorhabditis elegans
Human Chromosomes
Human Genome
Genetic Promoter Regions
DNA Repair
Open Reading Frames
DNA Damage

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Genomic sequence, structural organization, molecular evolution, and aberrant rearrangement of promyelocytic leukemia zinc finger gene. / Zhang, T.; Xiong, H.; Kan, L. X.; Zhang, C. K.; Jiao, X. F.; Fu, G.; Zhang, Q. H.; Lu, L.; Tong, J. H.; Gu, B. W.; Yu, M.; Liu, J. X.; Licht, J.; Waxman, S.; Zelent, Arthur Z; Chen, E.; Chen, S. J.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, No. 20, 28.09.1999, p. 11422-11427.

Research output: Contribution to journalArticle

Zhang, T, Xiong, H, Kan, LX, Zhang, CK, Jiao, XF, Fu, G, Zhang, QH, Lu, L, Tong, JH, Gu, BW, Yu, M, Liu, JX, Licht, J, Waxman, S, Zelent, AZ, Chen, E & Chen, SJ 1999, 'Genomic sequence, structural organization, molecular evolution, and aberrant rearrangement of promyelocytic leukemia zinc finger gene', Proceedings of the National Academy of Sciences of the United States of America, vol. 96, no. 20, pp. 11422-11427. https://doi.org/10.1073/pnas.96.20.11422
Zhang, T. ; Xiong, H. ; Kan, L. X. ; Zhang, C. K. ; Jiao, X. F. ; Fu, G. ; Zhang, Q. H. ; Lu, L. ; Tong, J. H. ; Gu, B. W. ; Yu, M. ; Liu, J. X. ; Licht, J. ; Waxman, S. ; Zelent, Arthur Z ; Chen, E. ; Chen, S. J. / Genomic sequence, structural organization, molecular evolution, and aberrant rearrangement of promyelocytic leukemia zinc finger gene. In: Proceedings of the National Academy of Sciences of the United States of America. 1999 ; Vol. 96, No. 20. pp. 11422-11427.
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abstract = "The promyelocytic leukemia zinc finger gene (PLZF) is involved in chromosomal translocation t(11;17) associated with acute promyelocytic leukemia. In this work, a 201-kilobase genomic DNA region containing the entire PLZF gene was sequenced. Repeated elements account for 19.83{\%}, and no obvious coding information other than PLZF is present over this region. PLZF contains six exons and five introns, and the exon organization corresponds well with protein domains. There are at least four alternative splicings (AS- I, -II, -III, and -IV) within exon 1. AS-I could be detected in most tissues tested whereas AS-II, -III, and -IV were present in the stomach, testis, and heart, respectively. Although splicing donor and acceptor signals at exon- intron boundaries for AS-I and exons 1-6 were classical (gt-ag), AS-II, -III, and -IV had atypical splicing sites. These alternative splicings, nevertheless, maintained the ORF and may encode isoforms with absence of important functional domains. In mRNA species without AS-I, there is a relatively long 5' UTR of 6.0 kilobases. A TATA box and several transcription factor binding sites were found in the putative promoter region upstream of the transcription start site. PLZF is a well conserved gene from Caenorhabditis elegans to human. PLZF paralogous sequences are found in human genome. The presence of two MLL/PLZF-like alignments on human chromosome 11q23 and 19 suggests a syntenic replication during evolution. The chromosomal breakpoints and joining sites in the index acute promyelocytic leukemia case with t(11;17) also were characterized, which suggests the involvement of DNA damage-repair mechanism.",
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AU - Zhang, C. K.

AU - Jiao, X. F.

AU - Fu, G.

AU - Zhang, Q. H.

AU - Lu, L.

AU - Tong, J. H.

AU - Gu, B. W.

AU - Yu, M.

AU - Liu, J. X.

AU - Licht, J.

AU - Waxman, S.

AU - Zelent, Arthur Z

AU - Chen, E.

AU - Chen, S. J.

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N2 - The promyelocytic leukemia zinc finger gene (PLZF) is involved in chromosomal translocation t(11;17) associated with acute promyelocytic leukemia. In this work, a 201-kilobase genomic DNA region containing the entire PLZF gene was sequenced. Repeated elements account for 19.83%, and no obvious coding information other than PLZF is present over this region. PLZF contains six exons and five introns, and the exon organization corresponds well with protein domains. There are at least four alternative splicings (AS- I, -II, -III, and -IV) within exon 1. AS-I could be detected in most tissues tested whereas AS-II, -III, and -IV were present in the stomach, testis, and heart, respectively. Although splicing donor and acceptor signals at exon- intron boundaries for AS-I and exons 1-6 were classical (gt-ag), AS-II, -III, and -IV had atypical splicing sites. These alternative splicings, nevertheless, maintained the ORF and may encode isoforms with absence of important functional domains. In mRNA species without AS-I, there is a relatively long 5' UTR of 6.0 kilobases. A TATA box and several transcription factor binding sites were found in the putative promoter region upstream of the transcription start site. PLZF is a well conserved gene from Caenorhabditis elegans to human. PLZF paralogous sequences are found in human genome. The presence of two MLL/PLZF-like alignments on human chromosome 11q23 and 19 suggests a syntenic replication during evolution. The chromosomal breakpoints and joining sites in the index acute promyelocytic leukemia case with t(11;17) also were characterized, which suggests the involvement of DNA damage-repair mechanism.

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