• Fulltext

       

        Click here to view fulltext PDF


      Permanent link:
      https://www.ias.ac.in/article/fulltext/jgen/086/02/0103-0109

    • Keywords

       

      mouse; gene expression; antisense; transcription; gene regulation.

    • Abstract

       

      There is a growing evidence, that antisense transcription might have a key role in a range of human diseases. Although predefined sense–antisense pairs were extensively studied, the antisense expression of the known sense genes is rarely investigated. We retrieved and correlated the expression of sense and antisense sequences of 1182 mouse transcripts to assess the prevalence and to find the characteristic pattern of antisense transcription. We contrasted three Affymetrix MGU74A version 1 mouse genome chips to six MGU74A version 2 chips. For these 1182 transcripts, the version 1 chips contain the antisense sequences of the transcripts presented on the version 2 chips. The original data was taken from the GEO database (GDS431 and GDS432). As the Affymetrix data are semiquantitative, the relative expression levels of antisense partners were analysed. We detected antisense transcription, although the average antisense expression is shifted towards smaller expression values (MGU74A version 1, 516; version 2, 1688). An inverse direct correlation between sense and antisense expression values could be observed at high expression values. At a very high relative expression—above 40,000—the Pearson correlation coefficient is getting closer to −1. Transcripts with high inverse expression ratio may be correlated to the investigated gene (major histocompatibility complex class II trans activator). The ratio of sense to antisense transcripts varied among different chromosomes; on chromosomes 14 and 1 the level of antisense expression was higher than that of sense. We conclude that antisense transcription is a common phenomenon in the mouse genome. The hypothesis of regulatory role of antisense transcripts is supported by the inverse antisense gene expression of highly expressed genes.

    • Author Affiliations

       

      Andras Györffy1 Pawel Surowiak2 Zsolt Tulassay1 Balazs Györffy3

      1. Joint Laboratory of the Hungarian Academy of Sciences and the Semmelweis University Budapest, Szentkirályi u. 46., H-1085 Budapest, Hungary
      2. Department of Histology and Embryology, University School of Medicine, ul. Chalubińskiego 6a, 50-356 Wroclaw, Poland
      3. Joint Research Laboratory for Pediatrics and Nephrology of the Hungarian Academy of Sciences and the Semmelweis University, Bokay u. 53/54, H-1083, Budapest, Hungary
    • Dates

       

© 2017 Indian Academy of Sciences, Bengaluru.