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Dosage compensation

About: Dosage compensation is a research topic. Over the lifetime, 1920 publications have been published within this topic receiving 124589 citations.


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Journal ArticleDOI
TL;DR: A novel class of noncoding RNAs that paint entire chromosomes are centrally involved in this process, and are key sites that target the X for dosage compensation.

42 citations

Journal ArticleDOI
01 Sep 1998-Heredity
TL;DR: Three RAPDs and one RFLP marker investigated suggest that sex-linked genes in the silkworm are not dosage compensated.
Abstract: To confirm whether sex-linked genes of the silkworm are dosage compensated or not, we investigated three RAPDs and one RFLP marker which have been mapped to the Z chromosome as candidate genes to test for dosage compensation. Northern blot analysis demonstrated that one of the RAPDs, T15.180a, is transcribed into several mRNAs in the embryo, midgut, Malpighian tubule, testis and ovary. Southern blot analysis revealed that T15.180a is present at one copy in the genome. Sequence data showed that T15.180a contained two open-reading frames (ORFs) separated by an intron of 605 bp. These ORFs encoded a possible polypeptide of 445 amino acids containing the proline cluster. These results suggested that T15.180a is part of a functional gene on the Z chromosome of the silkworm. We have called this gene T15, and compared its transcriptional level between males and females. Northern blot analysis showed that the level of T15 mRNA in males was twice that of females. For a more precise analysis, the levels of transcription from both alleles of T15 (T15P, T15C) were measured by the single-nucleotide primer extension (SNuPE) assay. The results indicated that the amount of transcription from each T15 allele in both sexes (male, T15P/T15C; female, T15P/W) was equivalent. All the results suggest that sex-linked genes in the silkworm are not dosage compensated.

42 citations

Journal ArticleDOI
TL;DR: Focusing on the best studied transcripts Xist and Tsix, a current perspective on chromosome wide gene regulation by non-coding RNAs is portrayed.
Abstract: Non-coding RNAs regulate dosage compensation in mammals by controlling transcriptional silencing of one of the two X chromosomes in females. The two major transcripts involved in this process are Xist and its antisense counterpart Tsix. Expression of Xist and Tsix from the X inactivation center is mutually exclusive. Xist expression triggers chromosome wide silencing of the X chromosome from which it is transcribed. Tsix is a repressor of Xist and is specifically expressed from the other X chromosome, maintaining its activity. Here, we review non-coding RNAs that have been implicated in X chromosome inactivation. Focusing on the best studied transcripts Xist and Tsix we portray a current perspective on chromosome wide gene regulation by non-coding RNAs.

42 citations

Journal ArticleDOI
TL;DR: It is reported that conserved GA repeat cis elements within the bidirectional histone3-histone4 promoter direct HLB formation in Drosophila are binding to GA repeat motifs, which promotes the formation of two distinct domains of coordinated gene activation located at different places in the genome.
Abstract: The conserved histone locus body (HLB) assembles prior to zygotic gene activation early during development and concentrates factors into a nuclear domain of coordinated histone gene regulation. Although HLBs form specifically at replication-dependent histone loci, the cis and trans factors that target HLB components to histone genes remained unknown. Here we report that conserved GA repeat cis elements within the bidirectional histone3-histone4 promoter direct HLB formation in Drosophila In addition, the CLAMP (chromatin-linked adaptor for male-specific lethal [MSL] proteins) zinc finger protein binds these GA repeat motifs, increases chromatin accessibility, enhances histone gene transcription, and promotes HLB formation. We demonstrated previously that CLAMP also promotes the formation of another domain of coordinated gene regulation: the dosage-compensated male X chromosome. Therefore, CLAMP binding to GA repeat motifs promotes the formation of two distinct domains of coordinated gene activation located at different places in the genome.

42 citations

Journal ArticleDOI
01 Feb 2006-Genetics
TL;DR: It is proposed that DCC-mediated site-specific upregulation of transcription is not the fate of all active X-linked genes in males, and that, independently of other MSL proteins, the RNA-helicase MLE might participate in general transcriptional regulation or RNA processing.
Abstract: 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.

42 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202330
202272
202183
202051
201980
201870