Transcription regulation of human chemokine receptor CCR3: Evidence for a rare TATA-less promoter structure conserved between Drosophila and humans

Sujata Vijh; Debora E. Dayhoff; Carol E. Wang; Zakaria Imam; Philip K. Ehrenberg; Nelson L. Michael

doi:10.1006/geno.2002.6801

Transcription regulation of human chemokine receptor CCR3: Evidence for a rare TATA-less promoter structure conserved between Drosophila and humans

Sujata Vijh, Debora E. Dayhoff, Carol E. Wang, Zakaria Imam, Philip K. Ehrenberg, Nelson L. Michael^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

The chemokine receptor CCR3 has a critical function in the pathogenesis of eosinophilic diseases and is an entry co-receptor for HIV-1. We describe here the genomic organization and general transcriptional control mechanism for the human gene CCR3. We identified six cDNA transcripts formed by alternative splicing of eight exons and seven introns. CCR3 contains a 37-bp core promoter domain (-3 to +34 relative to the transcription start point) lacking a TATA box but inclusive of an initiator sequence, a G at +24, and a downstream promoter element (DPE) at +28 to +33 common for Drosophila melanogaster but heretofore described for only two other human genes. Mutation of these elements significantly attenuates CCR3 transcription, as predicted by a model of RNA pol II engagement with DPE-containing Drosophila promoters. These results provide evidence for the functional conservation of a DPE-dependent, general transcription control mechanism between Drosophila and human genes.

Original language	English
Pages (from-to)	86-95
Number of pages	10
Journal	Genomics
Volume	80
Issue number	1
DOIs	https://doi.org/10.1006/geno.2002.6801
State	Published - 2002
Externally published	Yes

Keywords

AIDS
Allergy
Chemokines
Eosinophils
Molecular biology

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title = "Transcription regulation of human chemokine receptor CCR3: Evidence for a rare TATA-less promoter structure conserved between Drosophila and humans",

abstract = "The chemokine receptor CCR3 has a critical function in the pathogenesis of eosinophilic diseases and is an entry co-receptor for HIV-1. We describe here the genomic organization and general transcriptional control mechanism for the human gene CCR3. We identified six cDNA transcripts formed by alternative splicing of eight exons and seven introns. CCR3 contains a 37-bp core promoter domain (-3 to +34 relative to the transcription start point) lacking a TATA box but inclusive of an initiator sequence, a G at +24, and a downstream promoter element (DPE) at +28 to +33 common for Drosophila melanogaster but heretofore described for only two other human genes. Mutation of these elements significantly attenuates CCR3 transcription, as predicted by a model of RNA pol II engagement with DPE-containing Drosophila promoters. These results provide evidence for the functional conservation of a DPE-dependent, general transcription control mechanism between Drosophila and human genes.",

keywords = "AIDS, Allergy, Chemokines, Eosinophils, Molecular biology",

author = "Sujata Vijh and Dayhoff, {Debora E.} and Wang, {Carol E.} and Zakaria Imam and Ehrenberg, {Philip K.} and Michael, {Nelson L.}",

note = "Funding Information: W e thank Sheila Peel (W alter Reed Army Institute for Research) for critical reading of the manuscript and Ram Ramabhadran (Tranzyme, Inc.) for helpful discussion. S.V. was supported in part by NIH NRSA Individual Fellowship F32 AI09629-01A1. The views and opinions expressed herein are those of the authors and do not purport to reflect the official policy or position of the US Army or the Department of Defense. This work was supported in part by Cooperative Agreement No. DAMD17-93-V-3004, between the US Army Medical Research and Materiel Command and the US Military HIV Research Program.",

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AU - Dayhoff, Debora E.

AU - Wang, Carol E.

AU - Imam, Zakaria

AU - Ehrenberg, Philip K.

AU - Michael, Nelson L.

N1 - Funding Information: W e thank Sheila Peel (W alter Reed Army Institute for Research) for critical reading of the manuscript and Ram Ramabhadran (Tranzyme, Inc.) for helpful discussion. S.V. was supported in part by NIH NRSA Individual Fellowship F32 AI09629-01A1. The views and opinions expressed herein are those of the authors and do not purport to reflect the official policy or position of the US Army or the Department of Defense. This work was supported in part by Cooperative Agreement No. DAMD17-93-V-3004, between the US Army Medical Research and Materiel Command and the US Military HIV Research Program.

PY - 2002

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N2 - The chemokine receptor CCR3 has a critical function in the pathogenesis of eosinophilic diseases and is an entry co-receptor for HIV-1. We describe here the genomic organization and general transcriptional control mechanism for the human gene CCR3. We identified six cDNA transcripts formed by alternative splicing of eight exons and seven introns. CCR3 contains a 37-bp core promoter domain (-3 to +34 relative to the transcription start point) lacking a TATA box but inclusive of an initiator sequence, a G at +24, and a downstream promoter element (DPE) at +28 to +33 common for Drosophila melanogaster but heretofore described for only two other human genes. Mutation of these elements significantly attenuates CCR3 transcription, as predicted by a model of RNA pol II engagement with DPE-containing Drosophila promoters. These results provide evidence for the functional conservation of a DPE-dependent, general transcription control mechanism between Drosophila and human genes.

AB - The chemokine receptor CCR3 has a critical function in the pathogenesis of eosinophilic diseases and is an entry co-receptor for HIV-1. We describe here the genomic organization and general transcriptional control mechanism for the human gene CCR3. We identified six cDNA transcripts formed by alternative splicing of eight exons and seven introns. CCR3 contains a 37-bp core promoter domain (-3 to +34 relative to the transcription start point) lacking a TATA box but inclusive of an initiator sequence, a G at +24, and a downstream promoter element (DPE) at +28 to +33 common for Drosophila melanogaster but heretofore described for only two other human genes. Mutation of these elements significantly attenuates CCR3 transcription, as predicted by a model of RNA pol II engagement with DPE-containing Drosophila promoters. These results provide evidence for the functional conservation of a DPE-dependent, general transcription control mechanism between Drosophila and human genes.

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Transcription regulation of human chemokine receptor CCR3: Evidence for a rare TATA-less promoter structure conserved between Drosophila and humans

Abstract

Keywords

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