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Article Addendum

Transcription of mRNA-type long non-coding RNAs (mlonRNAs) disrupts chromatin array

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Pages 25-26 | Received 09 Nov 2008, Accepted 10 Nov 2008, Published online: 01 Feb 2009
 

Abstract

Eukaryotic transcriptome analyses have revealed that many transcripts are non-coding RNAs (ncRNAs). In addition, most relatively large (~several kb) polyadenylated mRNA type transcripts are transcribed from regions harboring little coding potential. However the role of such mRNA type long ncRNAs (mlonRNAs) is mostly unknown and has been a matter of debate. Recently, we showed that cascade of RNA polymerase II (RNAPII)-mediated transcriptional initiation of mlonRNA causes stepwise disruption of local chromatin array at the fission yeast Schizosaccharomyces pombe fbp1+ promoter region. Here, we hypothesize that RNAPII transcription of mlonRNA disrupt chromatin array possibly collaborating with histone acetylation mechanism. In addition, conserved action of Atf1, a transcriptional activator, and Tup11-Tup12 corepressors along mlonRNA transcription mediated chromatin regulation is suggested. This idea provides new insight into the biological meaning of mlonRNAs found in various eukaryotes.

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Figures and Tables

Figure 1 A model representing mlonRNA transcription disrupts chromatin array. (A) In glucose rich condition, rare mlonRNA is transcribed from a site far upstream from the authentic fbp1+ promoter, but does not initiate the robust activation of fbp1+ transcription at the promoter due to the Tup-dependent repressive chromatin structure. (B) Upon glucose starvation, Atf1 binds upper binding site (carrying CRE sequence). Atf1 activates progressive mlonRNA initiations, and this mlonRNA transcription overcomes the repressive role of the Tup proteins. (C) RNAPII traveling along upper fbp1+ region disrupts chromatin array possibly collaborating with HAT activity.

Figure 1 A model representing mlonRNA transcription disrupts chromatin array. (A) In glucose rich condition, rare mlonRNA is transcribed from a site far upstream from the authentic fbp1+ promoter, but does not initiate the robust activation of fbp1+ transcription at the promoter due to the Tup-dependent repressive chromatin structure. (B) Upon glucose starvation, Atf1 binds upper binding site (carrying CRE sequence). Atf1 activates progressive mlonRNA initiations, and this mlonRNA transcription overcomes the repressive role of the Tup proteins. (C) RNAPII traveling along upper fbp1+ region disrupts chromatin array possibly collaborating with HAT activity.

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