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

Kotlikova, Irina V.; Demakova, Olga V.; Semeshin, V. F.; Shloma, Victor V.; Boldyreva, Lidiya V.; Kuroda, Mitzi I.; Жимулев, И. Ф.

doi:10.1534/genetics.105.045286

Cited by 39 publications

(35 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, the comparison of the MSL-1-binding pattern with transcription-associated factors such as Spt-5, Spt-6, and S5-P PolII on intact polytene chromosomes also did not reveal a strong overlap between these proteins and MSL-1. These results are also consistent with recent observations (Kotlikova et al 2006) that these transcription-associated factors localize both in bands enriched in MSL-1 and in bands depleted of MSL-1.…”

Section: Targeting Of the Msl Complex On The X Chromosomesupporting

confidence: 93%

X-chromosome-wide profiling of MSL-1 distribution and dosage compensation inDrosophila

et al. 2006

View full text Add to dashboard Cite

In Drosophila, dosage compensation is achieved by a twofold up-regulation of the male X-linked genes and requires the association of the male-specific lethal complex (MSL) on the X chromosome. How the MSL complex is targeted to X-linked genes and whether its recruitment at a local level is necessary and sufficient to ensure dosage compensation remain poorly understood. Here we report the MSL-1-binding profile along the male X chromosome in embryos and male salivary glands isolated from third instar larvae using chromatin immunoprecipitation ( [Keywords: MSL; X chromosome; chromatin; dosage compensation; transcription] Supplemental material is available at http://www.genesdev.org.

show abstract

Section: Targeting Of the Msl Complex On The X Chromosomesupporting

confidence: 93%

X-chromosome-wide profiling of MSL-1 distribution and dosage compensation inDrosophila

et al. 2006

View full text Add to dashboard Cite

show abstract

“…Surprisingly, ∼25% of the genes binding pol II (374/1412) did not also bind MSL1, suggesting that they may not be dosage compensated, or compensated post-transcriptionally, although we cannot exclude signals from genes expressed only in females. Thus, transcription alone appears insufficient to attract the DCC, in agreement with recent observations of pol II and DCC binding to polytene chromosomes (Kotlikova et al 2006). Also of interest is the high number (140) of protein-coding genes that bind MSL1 but have no detectable pol II (∼12% of genes binding MSL1).…”

Section: Transcription Is Not Sufficient To Recruit the DCCsupporting

confidence: 89%

“…In this context, the genes found in embryos to be binding MSL1 and not polymerase may be examples of genes already expressed and since silenced, or genes awaiting activation. In Drosophila larvae, conflicting reports observed either a sustained pattern of MSL1 and MSL3 binding to polytene chromosomes (Kotlikova et al 2006), or subtle changes throughout larval development (Sass et al 2003). The steady expression levels observed throughout development for many embryonic DCC-target genes in this study suggests that those genes will be expressed constitutively.…”

Section: Dna Sequence Elements May Attract the DCC To Target Genesmentioning

confidence: 52%

Chromosome-wide gene-specific targeting of theDrosophiladosage compensation complex

Gilfillan¹,

Straub²,

Wit³

et al. 2006

Genes Dev.

147

209

View full text Add to dashboard Cite

The dosage compensation complex (DCC) of Drosophila melanogaster is capable of distinguishing the single male X from the other chromosomes in the nucleus. It selectively interacts in a discontinuous pattern with much of the X chromosome. How the DCC identifies and binds the X, including binding to the many genes that require dosage compensation, is currently unknown. To identify bound genes and attempt to isolate the targeting cues, we visualized male-specific lethal 1 (MSL1) protein binding along the X chromosome by combining chromatin immunoprecipitation with high-resolution microarrays. More than 700 binding regions for the DCC were observed, encompassing more than half the genes found on the X chromosome. In addition, several rare autosomal binding sites were identified. Essential genes are preferred targets, and genes binding high levels of DCC appear to experience the most compensation (i.e., greatest increase in expression). DCC binding clearly favors genes over intergenic regions, and binds most strongly to the 3 end of transcription units. Within the targeted genes, the DCC exhibits a strong preference for exons and coding sequences. Our results demonstrate gene-specific binding of the DCC, and identify several sequence elements that may partly direct its targeting.[Keywords: Transcription; histone modification; chromatin remodeling; MSL complex; microarray; gene expression] Supplemental material is available at http://www.genesdev.org.

show abstract

“…MLE is enriched on the male X chromosome but also found at sites of active transcription in males and females (Kotlikova et al 2006). MOF is an integral member of the DCC and is enriched on the male X chromosome.…”

mentioning

confidence: 99%

Coordinated Regulation of Heterochromatic Genes inDrosophila melanogasterMales

et al. 2009

View full text Add to dashboard Cite

Dosage compensation modifies the chromatin of X-linked genes to assure equivalent expression in sexes with unequal X chromosome dosage. In Drosophila dosage compensation is achieved by increasing expression from the male X chromosome. The ribonucleoprotein dosage compensation complex (DCC) binds hundreds of sites along the X chromosome and modifies chromatin to facilitate transcription. Loss of roX RNA, an essential component of the DCC, reduces expression from X-linked genes. Surprisingly, loss of roX RNA also reduces expression from genes situated in proximal heterochromatin and on the small, heterochromatic fourth chromosome. Mutation of some, but not all, of the genes encoding DCC proteins produces a similar effect. Reduction of roX function suppresses position effect variegation (PEV), revealing functional alteration in heterochromatin. The effects of roX mutations on heterochromatic gene expression and PEV are limited to males. A sex-limited role for the roX RNAs in autosomal gene expression was unexpected. We propose that this reflects a difference in the heterochromatin of males and females, which serves to accommodate the heterochromatic Y chromosome present in the male nucleus. roX transcripts may thus participate in two distinct regulatory systems that have evolved in response to highly differentiated sex chromosomes: compensation of X-linked gene dosage and modulation of heterochromatin.

show abstract

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

Cited by 39 publications

References 72 publications

X-chromosome-wide profiling of MSL-1 distribution and dosage compensation inDrosophila

X-chromosome-wide profiling of MSL-1 distribution and dosage compensation inDrosophila

Chromosome-wide gene-specific targeting of theDrosophiladosage compensation complex

Coordinated Regulation of Heterochromatic Genes inDrosophila melanogasterMales

Contact Info

Product

Resources

About