Dosage compensation and intercalary heterochromatin in X chromosomes of Drosophila melanogaster

Alekseyenko, Artyom A.; Demakova, Olga V.; Belyaeva, E. S.; Makarevich, Grigorii F.; Kotlikova, Irina V.; Nöthiger, Rolf; Жимулев, И. Ф.

doi:10.1007/s00412-002-0191-7

Cited by 9 publications

(4 citation statements)

References 30 publications

(33 reference statements)

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“…This correlation seems to reflect a threshold reaction:~60%-70% of the normal male level of MSL2 (in w; msl3 p [w + , H83M2-61]/TM6 females) provided establishment of a male-like structure along the female X chromosomes. This observation is coincident with our recent data on the effect of MSL complex levels on DNA replication in the regions of intercalary heterochromatin distributed along the X chromosome (Alekseyenko et al 2002). DNA replication is reduced in the 11A6-9 region of SXB1-2 females (as in wild-type females), while this underreplication is completely suppressed in w; msl3 p [w + , H83M2-61]/TM6 females (as is typical of wild-type males), probably due to MSL complex-mediated chromatin remodeling.…”

Section: Discussionsupporting

confidence: 91%

The MSL complex levels are critical for its correct targeting to the chromosomes in Drosophila melanogaster

et al. 2003

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In Drosophila, dosage compensation requires assembly of the Male Specific Lethal (MSL) protein complex for doubling transcription of most X-linked genes in males. The recognition of the X chromosome by the MSL complex has been suggested to include initial assembly at approximately 35 chromatin entry sites and subsequent spreading of mature complexes in cis to numerous additional sites along the chromosome. To understand this process further we examined MSL patterns in a range of wild-type and mutant backgrounds producing different amounts of MSL components. Our data support a model in which MSL complex binding to the X is directed by a hierarchy of target sites that display different affinities for the MSL proteins. Chromatin entry sites differ in their ability to provide local intensive binding of complexes to adjacent regions, and need high MSL complex titers to achieve this. We also mapped a set of definite autosomal regions (approximately 70) competent to associate with the functional MSL complex in wild-type males. Overexpression of both MSL1 and MSL2 stabilizes this binding and results in inappropriate MSL binding to the chromocenter and the 4th chromosome. Thus, wild-type MSL complex titers are critical for correct targeting to the X chromosome.

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Section: Discussionsupporting

confidence: 91%

The MSL complex levels are critical for its correct targeting to the chromosomes in Drosophila melanogaster

et al. 2003

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“…Such changes are explained by earlier replication of the majority of IH sites, which complete replication at the same time as normal euchromatic regions, at the stage of continuous labeling. A similar shift in timing was previously found for the wild-type male X chromosome and was attributed to chromatin changes related to the dosage compensation mechanisms (for discussion see Alekseyenko et al 2002). The SuUR protein is located exclusively in regions of late replication and is probably involved in processes of late replication, since the mutation of this gene does not evoke other phenotypic changes and does not influence the duration of development or the number of polytenization rounds.…”

Section: Discussionmentioning

confidence: 52%

Influence of the SuUR gene on intercalary heterochromatin in Drosophila melanogaster polytene chromosomes

et al. 2003

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Salivary gland polytene chromosomes of Drosophila melanogaster have a reproducible set of intercalary heterochromatin (IH) sites, characterized by late DNA replication, underreplicated DNA, breaks and frequent ectopic contacts. The SuUR mutation has been shown to suppress underreplication, and wild-type SuUR protein is found at late-replicating IH sites and in pericentric heterochromatin. Here we show that the SuUR gene influences all four IH features. The SuUR mutation leads to earlier completion of DNA replication. Using transgenic strains with two, four or six additional SuUR(+) doses (4-8xSuUR(+)) we show that wild-type SuUR is an enhancer of DNA underreplication, causing many late-replicating sites to become underreplicated. We map the underreplication sites and show that their number increases from 58 in normal strains (2xSuUR(+)) to 161 in 4-8xSuUR(+) strains. In one of these new sites (1AB) DNA polytenization decreases from 100% in the wild type to 51%-85% in the 4xSuUR (+) strain. In the 4xSuUR(+) strain, 60% of the weak points coincide with the localization of Polycomb group (PcG) proteins. At the IH region 89E1-4 (the Bithorax complex), a typical underreplication site, the degree of underreplication increases with four doses of SuUR(+) but the extent of the underreplicated region is the same as in wild type and corresponds to the region containing PcG binding sites. We conclude that the polytene chromosome regions known as IH are binding sites for SuUR protein and in many cases PcG silencing proteins. We propose that these stable silenced regions are late replicated and, in the presence of SuUR protein, become underreplicated.

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“…Accordingly, in females having ectopic dosage compensation induced, the DCC gap corresponding to the intercalary heterochromatin region on the polytene X demonstrated a greater extent of both polytenization and replication than in the wild type. This clearly correlated with the higher local concentrations of the DCC in neighboring areas (Alekseyenko et al 2002). Thus, despite the fact that the DCC-mediated site-specific histone acetylation pattern correlates with an increase in transcription of the underlying sequences (Akhtar et al 2000;Henry et al 2001;Smith et al 2001), we believe it would be more accurate to suggest that there is no common scenario of dosage compensation for all the X-linked genes.…”

Section: Discussionmentioning

confidence: 86%

The Drosophila Dosage Compensation Complex Binds to Polytene Chromosomes Independently of Developmental Changes in Transcription

et al. 2006

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In Drosophila, the dosage compensation complex (DCC) mediates upregulation of transcription from the single male X chromosome. Despite coating the polytene male X, the DCC pattern looks discontinuous and probably reflects DCC dynamic associations with genes active at a given moment of development in a salivary gland. To test this hypothesis, we compared binding patterns of the DCC and of the elongating form of RNA polymerase II (PolIIo). We found that, unlike PolIIo, the DCC demonstrates a stable banded pattern throughout larval development and escapes binding to a subset of transcriptionally active areas, including developmental puffs. Moreover, these proteins are not completely colocalized at the electron microscopy level. These data combined imply that simple recognition of PolII machinery or of general features of active chromatin is either insufficient or not involved in DCC recruitment to its targets. We propose that DCC-mediated site-specific upregulation of transcription is not the fate of all active X-linked genes in males. Additionally, we found that DCC subunit MLE associates dynamically with developmental and heat-shock-induced puffs and, surprisingly, with those developing within DCC-devoid regions of the male X, thus resembling the PolIIo pattern. These data imply that, independently of other MSL proteins, the RNA-helicase MLE might participate in general transcriptional regulation or RNA processing.

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Dosage compensation and intercalary heterochromatin in X chromosomes of Drosophila melanogaster

Cited by 9 publications

References 30 publications

The MSL complex levels are critical for its correct targeting to the chromosomes in Drosophila melanogaster

The MSL complex levels are critical for its correct targeting to the chromosomes in Drosophila melanogaster

Influence of the SuUR gene on intercalary heterochromatin in Drosophila melanogaster polytene chromosomes

The Drosophila Dosage Compensation Complex Binds to Polytene Chromosomes Independently of Developmental Changes in Transcription

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