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Epigenetics and targeting mechanisms in Drosophila melanogaster
Umeå University, Faculty of Science and Technology, Department of Molecular Biology (Faculty of Science and Technology). (Jan Larsson)
2015 (English)Doctoral thesis, comprehensive summary (Other academic)
Place, publisher, year, edition, pages
Umeå: Umeå University , 2015. , 65 p.
Keyword [en]
Drosophila, Aneuplodies, HP1a, POF, MSL, non-coding RNAs
National Category
Biological Sciences
Research subject
Genetics
Identifiers
URN: urn:nbn:se:umu:diva-102890ISBN: 978-91-7601-267-3 (print)OAI: oai:DiVA.org:umu-102890DiVA: diva2:811006
Public defence
2015-06-04, Astrid Fagraeus Hörsal A 103 Unod R 1, NUS – Norrlands universitetssjukhus, Umeå, 09:00 (English)
Opponent
Supervisors
Available from: 2015-05-13 Created: 2015-05-09 Last updated: 2015-05-18Bibliographically approved
List of papers
1. Buffering and proteolysis are induced by segmental monosomy in Drosophila melanogaster
Open this publication in new window or tab >>Buffering and proteolysis are induced by segmental monosomy in Drosophila melanogaster
2012 (English)In: Nucleic Acids Research, ISSN 0305-1048, E-ISSN 1362-4962, Vol. 40, no 13, 5926-5937 p.Article in journal (Refereed) Published
Abstract [en]

Variation in the number of individual chromosomes (chromosomal aneuploidy) or chromosome segments (segmental aneuploidy) is associated with developmental abnormalities and reduced fitness in all species examined; it is the leading cause of miscarriages and mental retardation and a hallmark of cancer. However, despite their documented importance in disease, the effects of aneuploidies on the transcriptome remain largely unknown. We have examined the expression effects of seven heterozygous chromosomal deficiencies, both singly and in all pairwise combinations, in Drosophila melanogaster. The results show that genes in one copy are buffered, i.e. expressed more strongly than the expected 50% of wild-type level, the buffering is general and not influenced by other monosomic regions. Furthermore, long genes are significantly more highly buffered than short genes and gene length appears to be the primary determinant of the buffering degree. For short genes the degree of buffering depends on expression level and expression pattern. Furthermore, the results show that in deficiency heterozygotes the expression of genes involved in proteolysis is enhanced and negatively correlates with the degree of buffering. Thus, enhanced proteolysis appears to be a general response to aneuploidy.

Place, publisher, year, edition, pages
Oxford: Oxford University Press, 2012
National Category
Genetics
Research subject
Genetics
Identifiers
urn:nbn:se:umu:diva-53361 (URN)10.1093/nar/gks245 (DOI)000306970700018 ()22434883 (PubMedID)
Available from: 2012-03-23 Created: 2012-03-23 Last updated: 2017-12-07Bibliographically approved
2. HP1a Recruitment to Promoters Is Independent of H3K9 Methylation in Drosophila melanogaster
Open this publication in new window or tab >>HP1a Recruitment to Promoters Is Independent of H3K9 Methylation in Drosophila melanogaster
2012 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 8, no 11, e1003061- p.Article in journal (Refereed) Published
Abstract [en]

Heterochromatin protein 1 (HP1) proteins, recognized readers of the heterochromatin mark methylation of histone H3 lysine 9 (H3K9me), are important regulators of heterochromatin-mediated gene silencing and chromosome structure. In Drosophila melanogaster three histone lysine methyl transferases (HKMTs) are associated with the methylation of H3K9: Su(var)3-9, Setdb1, and G9a. To probe the dependence of HP1a binding on H3K9me, its dependence on these three HKMTs, and the division of labor between the HKMTs, we have examined correlations between HP1a binding and H3K9me patterns in wild type and null mutants of these HKMTs. We show here that Su(var)3-9 controls H3K9me-dependent binding of HP1a in pericentromeric regions, while Setdb1 controls it in cytological region 2L:31 and (together with POF) in chromosome 4. HP1a binds to the promoters and within bodies of active genes in these three regions. More importantly, however, HP1a binding at promoters of active genes is independent of H3K9me and POF. Rather, it is associated with heterochromatin protein 2 (HP2) and open chromatin. Our results support a hypothesis in which HP1a nucleates with high affinity independently of H3K9me in promoters of active genes and then spreads via H3K9 methylation and transient looping contacts with those H3K9me target sites.

National Category
Genetics
Research subject
Genetics
Identifiers
urn:nbn:se:umu:diva-61705 (URN)10.1371/journal.pgen.1003061 (DOI)000311891600046 ()23166515 (PubMedID)
Available from: 2012-11-23 Created: 2012-11-23 Last updated: 2017-12-07Bibliographically approved
3. Non-coding roX RNAs prevent the binding of the MSL-complex to heterochromatic regions
Open this publication in new window or tab >>Non-coding roX RNAs prevent the binding of the MSL-complex to heterochromatic regions
Show others...
2014 (English)In: PLoS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 10, no 12, e1004865- p.Article in journal (Refereed) Published
Abstract [en]

Long non-coding RNAs contribute to dosage compensation in both mammals and Drosophila by inducing changes in the chromatin structure of the X-chromosome. In Drosophila melanogaster, roX1 and roX2 are long non-coding RNAs that together with proteins form the male-specific lethal (MSL) complex, which coats the entire male X-chromosome and mediates dosage compensation by increasing its transcriptional output. Studies on polytene chromosomes have demonstrated that when both roX1 and roX2 are absent, the MSL-complex becomes less abundant on the male X-chromosome and is relocated to the chromocenter and the 4thchromosome. Here we address the role of roX RNAs in MSL-complex targeting and the evolution of dosage compensation in Drosophila. We performed ChIP-seq experiments which showed that MSL-complex recruitment to high affinity sites (HAS) on the X-chromosome is independent of roX and that the HAS sequence motif is conserved in D. simulans. Additionally, a complete and enzymatically active MSL-complex is recruited to six specific genes on the 4thchromosome. Interestingly, our sequence analysis showed that in the absence of roX RNAs, the MSL-complex has an affinity for regions enriched in Hoppel transposable elements and repeats in general. We hypothesize that roX mutants reveal the ancient targeting of the MSL-complex and propose that the role of roX RNAs is to prevent the binding of the MSL-complex to heterochromatin.

National Category
Biochemistry and Molecular Biology Genetics Bioinformatics and Systems Biology
Identifiers
urn:nbn:se:umu:diva-93046 (URN)10.1371/journal.pgen.1004865 (DOI)000346649900060 ()25501352 (PubMedID)2-s2.0-84919667251 (Scopus ID)
Funder
Swedish Research Council, 621-2012-2165
Note

Originally included in thesis in manuscript form.

Available from: 2014-09-11 Created: 2014-09-11 Last updated: 2017-12-05Bibliographically approved
4. The Male-Specific Lethal complex interacts with non-roX RNAs in Drosophila melanogaster
Open this publication in new window or tab >>The Male-Specific Lethal complex interacts with non-roX RNAs in Drosophila melanogaster
(English)Manuscript (preprint) (Other academic)
Keyword
Drosophila, Dosage Compensation, non-coding RNAs
National Category
Natural Sciences
Research subject
Genetics
Identifiers
urn:nbn:se:umu:diva-102889 (URN)
Available from: 2015-05-09 Created: 2015-05-09 Last updated: 2015-05-12Bibliographically approved

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Figueiredo, Margarida

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