The transcriptome profile of human trisomy 21 blood cells.


Journal

Human genomics
ISSN: 1479-7364
Titre abrégé: Hum Genomics
Pays: England
ID NLM: 101202210

Informations de publication

Date de publication:
01 05 2021
Historique:
received: 07 01 2021
accepted: 14 04 2021
entrez: 2 5 2021
pubmed: 3 5 2021
medline: 5 2 2022
Statut: epublish

Résumé

Trisomy 21 (T21) is a genetic alteration characterised by the presence of an extra full or partial human chromosome 21 (Hsa21) leading to Down syndrome (DS), the most common form of intellectual disability (ID). It is broadly agreed that the presence of extra genetic material in T21 gives origin to an altered expression of genes located on Hsa21 leading to DS phenotype. The aim of this study was to analyse T21 and normal control blood cell gene expression profiles obtained by total RNA sequencing (RNA-Seq). The results were elaborated by the TRAM (Transcriptome Mapper) software which generated a differential transcriptome map between human T21 and normal control blood cells providing the gene expression ratios for 17,867 loci. The obtained gene expression profiles were validated through real-time reverse transcription polymerase chain reaction (RT-PCR) assay and compared with previously published data. A post-analysis through transcriptome mapping allowed the identification of the segmental (regional) variation of the expression level across the whole genome (segment-based analysis of expression). Interestingly, the most over-expressed genes encode for interferon-induced proteins, two of them (MX1 and MX2 genes) mapping on Hsa21 (21q22.3). The altered expression of genes involved in mitochondrial translation and energy production also emerged, followed by the altered expression of genes encoding for the folate cycle enzyme, GART, and the folate transporter, SLC19A1. The alteration of these pathways might be linked and involved in the manifestation of ID in DS.

Sections du résumé

BACKGROUND
Trisomy 21 (T21) is a genetic alteration characterised by the presence of an extra full or partial human chromosome 21 (Hsa21) leading to Down syndrome (DS), the most common form of intellectual disability (ID). It is broadly agreed that the presence of extra genetic material in T21 gives origin to an altered expression of genes located on Hsa21 leading to DS phenotype. The aim of this study was to analyse T21 and normal control blood cell gene expression profiles obtained by total RNA sequencing (RNA-Seq).
RESULTS
The results were elaborated by the TRAM (Transcriptome Mapper) software which generated a differential transcriptome map between human T21 and normal control blood cells providing the gene expression ratios for 17,867 loci. The obtained gene expression profiles were validated through real-time reverse transcription polymerase chain reaction (RT-PCR) assay and compared with previously published data. A post-analysis through transcriptome mapping allowed the identification of the segmental (regional) variation of the expression level across the whole genome (segment-based analysis of expression). Interestingly, the most over-expressed genes encode for interferon-induced proteins, two of them (MX1 and MX2 genes) mapping on Hsa21 (21q22.3). The altered expression of genes involved in mitochondrial translation and energy production also emerged, followed by the altered expression of genes encoding for the folate cycle enzyme, GART, and the folate transporter, SLC19A1.
CONCLUSIONS
The alteration of these pathways might be linked and involved in the manifestation of ID in DS.

Identifiants

pubmed: 33933170
doi: 10.1186/s40246-021-00325-4
pii: 10.1186/s40246-021-00325-4
pmc: PMC8088681
doi:

Substances chimiques

MX1 protein, human 0
MX2 protein, human 0
Myxovirus Resistance Proteins 0
Reduced Folate Carrier Protein 0
SLC19A1 protein, human 0
Phosphoribosylglycinamide Formyltransferase EC 2.1.2.2
Carbon-Nitrogen Ligases EC 6.3.-
GART protein, human EC 6.3.4.13

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

25

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Auteurs

Francesca Antonaros (F)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Rossella Zenatelli (R)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.
Current Address: Department of Molecular and Translational Medicine (DMMT), University of Brescia, Viale Europa 11, 24123, Brescia, BS, Italy.

Giulia Guerri (G)

MAGI'S Lab, Via delle Maioliche 57/D, 38068, Rovereto, TN, Italy.

Matteo Bertelli (M)

MAGI'S Lab, Via delle Maioliche 57/D, 38068, Rovereto, TN, Italy.

Chiara Locatelli (C)

Neonatology Unit, St. Orsola-Malpighi Polyclinic, Via Massarenti 9, 40138, Bologna, BO, Italy.

Beatrice Vione (B)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Francesca Catapano (F)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.
Current Address: Department of Medical Biotechnologies, University of Siena, Strada delle Scotte, 4, 53100, Siena, SI, Italy.

Alice Gori (A)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Lorenza Vitale (L)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Maria Chiara Pelleri (MC)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Giuseppe Ramacieri (G)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Guido Cocchi (G)

Neonatology Unit, St. Orsola-Malpighi Polyclinic, Department of Medical and Surgical Sciences (DIMEC), University of Bologna, Via Massarenti 9, 40138, Bologna, BO, Italy.

Pierluigi Strippoli (P)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

Maria Caracausi (M)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy. maria.caracausi2@unibo.it.

Allison Piovesan (A)

Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Unit of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro 8, 40126, Bologna, BO, Italy.

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