Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Prokesch, A; Bogner-Strauss, JG; Hackl, H; Rieder, D; Neuhold, C; Walenta, E; Krogsdam, A; Scheideler, M; Papak, C; Wong, WC; Vinson, C; Eisenhaber, F; Trajanoski, Z.
Arxes: retrotransposed genes required for adipogenesis.
Nucleic Acids Res. 2011; 39(8): 3224-3239. Doi: 10.1093/nar/gkq1289 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz
Prokesch Andreas
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Abstract:
Retrotransposed sequences arise from messenger RNAs (mRNAs) that have been reinserted into genomic DNA by reverse transcription. Usually, these sequences are embedded in dormant regions, collect missense mutations over time and constitute processed, nonfunctional pseudogenes. There are thousands of processed pseudogenes in the mouse and human genome. Here, we report evidence for two paralog genes (termed Arxes1 and Arxes2), which arose by retrotransposition of the signal peptidase Spcs3 followed by a segmental duplication event. They gained a functional promoter that we show to be transactivated by adipogenic transcription factors. We further show that the Arxes mRNAs are highly expressed in adipose tissue and strongly upregulated during adipogenesis in different cell models. Additionally, their expression is elevated by an anti-diabetic agent in vitro and in vivo. Importantly, we provide evidence that the Arxes genes are translated and that the proteins are located in the endoplasmic reticulum. Although the sequence similarity and subcellular location are reminiscent of their parental gene, our data suggest that the Arxes have developed a different function, since their expression is required for adipogenesis, whereas Spcs3 is dispensable. In summary, we report retrotransposed-duplicated genes that evolved from a parental gene to function in a tissue and adipogenesis-specific context.
Find related publications in this database (using NLM MeSH Indexing)
3T3-L1 Cells -
Adipogenesis - genetics
Adipose Tissue - metabolism
Animals -
CCAAT-Enhancer-Binding Proteins - metabolism
Cells, Cultured -
Gene Expression Profiling -
Genomics -
Hypoglycemic Agents - pharmacology
Male -
Mice -
Mice, Inbred C57BL -
Osteoblasts - cytology
Osteogenesis -
PPAR gamma - metabolism
Peptide Hydrolases - genetics Peptide Hydrolases - metabolism Peptide Hydrolases - physiology
RNA Interference -
RNA, Messenger - metabolism
Retroelements -
Sequence Analysis, DNA -
Up-Regulation -

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