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msl2 mRNA is bound by free nuclear MSL complex in Drosophila melanogaster
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology).
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology).
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology). (Computational Life Science Cluster (CLiC))
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology).
2011 (English)In: Nucleic Acids Research, ISSN 0305-1048, E-ISSN 1362-4962, Vol. 39, no 15, 6428-6439 p.Article in journal (Refereed) Published
Abstract [en]

In Drosophila, the global increase in transcription from the male X chromosome to compensate for its monosomy is mediated by the male-specific lethal (MSL) complex consisting of five proteins and two non-coding RNAs, roX1 and roX2. After an initial sequence-dependent recognition by the MSL complex of 150-300 high affinity sites, the spread to the majority of the X-linked genes depends on local MSL-complex concentration and active transcription. We have explored whether any additional RNA species are associated with the MSL complex. No additional roX RNA species were found, but a strong association was found between a spliced and poly-adenylated msl2 RNA and the MSL complex. Based on our results, we propose a model in which a non-chromatin-associated partial or complete MSL-complex titrates newly transcribed msl2 mRNA and thus regulates the amount of available MSL complex by feedback. This represents a novel mechanism in chromatin structure regulation.

Place, publisher, year, edition, pages
Oxford Journals , 2011. Vol. 39, no 15, 6428-6439 p.
National Category
Genetics
Research subject
Genetics
Identifiers
URN: urn:nbn:se:umu:diva-43980DOI: 10.1093/nar/gkr236PubMedID: 21551218OAI: oai:DiVA.org:umu-43980DiVA: diva2:417503
Funder
Swedish Research Council
Available from: 2011-05-17 Created: 2011-05-17 Last updated: 2017-12-11
In thesis
1. Chromosome-wide gene regulatory mechanisms in Drosophila melanogaster
Open this publication in new window or tab >>Chromosome-wide gene regulatory mechanisms in Drosophila melanogaster
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

In Drosophila there are two different chromosome-wide targeting systems, the dosage compensation system that equalizes the transcriptional output from X-linked genes between males and females, and the regulation of the 4th chromosome mediated by the POF protein.

 

The best studied of these two mechanisms is the dosage compensation system. To attain dosage compensation in Drosophila at least five different proteins, encoded by the male-specific lethal genes msl1, msl2, msl3, mle and mof, are required. These proteins together with two non-coding RNAs (roX1 and roX2) form a dosage compensation complex (MSL complex), which binds exclusively to the X chromosome in Drosophila males and up-regulates the transcription approximately two times.

 

In this thesis I show that roX1 and roX2 are most likely the only non-coding RNAs within the MSL complex. As expected, the roX transcripts were enriched within the MSL complex. Interestingly, one additional transcript was identified within the MSL complex. This transcript did not associate with the X chromosome and is therefore not believed to be involved in up-regulation of the X-linked genes. This transcript encodes for the rate limiting component in the MSL complex, the MSL2 protein. A model is proposed in which free, partial or complete, MSL complex feed-back regulates the amount of msl2 transcript, and thereby limits the MSL complex production.

 

The second chromosome-wide regulatory system in flies acts on an autosome, the heterochromatic 4th chromosome. This regulation is a balancing mechanism between at least two different proteins, the chromosome 4 specific protein painting of fourth (POF) and heterochromatin protein 1 (HP1). POF binds to nascent RNAs transcribed from the 4th chromosome and HP1 target the same set of genes at the chromatin level. POF stimulates the transcribed genes, while HP1 represses them; together they create the most optimal condition for these genes. This type of balancing mechanism may be a more general way to fine-tune transcription at a chromosome-wide level and raises the question about autosomal gene regulation as a general mechanism.

Place, publisher, year, edition, pages
Umeå: Arkitektkopia, 2010. 75 p.
Keyword
Chromatin structure, Drosophila, POF, disage compensation, gene expression, MSL, heterochromatin
National Category
Genetics
Research subject
Genetics
Identifiers
urn:nbn:se:umu:diva-33928 (URN)978-91-7459-017-3 (ISBN)
Public defence
2010-06-04, Major Groove, byggnad 6L, Umeå Universitet, Umeå, 13:00 (English)
Opponent
Supervisors
Available from: 2010-05-12 Created: 2010-05-10 Last updated: 2011-05-17Bibliographically approved

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Johansson, Anna-MiaAllgardsson, AndersStenberg, PerLarsson, Jan

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