scholarly journals Author response: Condensin controls recruitment of RNA polymerase II to achieve nematode X-chromosome dosage compensation

2013 ◽  
Author(s):  
William S Kruesi ◽  
Leighton J Core ◽  
Colin T Waters ◽  
John T Lis ◽  
Barbara J Meyer
1981 ◽  
Vol 47 (1) ◽  
pp. 295-309
Author(s):  
R.N. Chatterjee ◽  
A.S. Mukherjee

The results of examination of the template activity of the fixed polytene chromosomes of Drosophila hydei, monitored by 3H-UTP, under in situ assay conditions, upon the use of endogenous Drosophila polymerase, exogenous Escherichia coli RNA polymerase (holoenzyme) and exogenous Drosophila RNA polymerase II (or B) have been presented. Analysis of the data reveals that the transcription patterns with the 3 enzymes are not strictly comparable with the pattern obtained under in vivo conditions. Yet, with each of the 3 conditions of assay, there is a reasonable concordance between the template activity on the single X chromosome of the male and the paired Xs of the female, as observed under in vivo. There is also, in every case, a high positive correlation between the 3H-UMP incorporation into the X chromosome and that into a specific autosome. A site-wise analysis of 3H-UMP labelling under the 3 assay conditions also reveals that for most of the regions, the sites which are highly active in vivo also show high labelling in situ, and the proportionally is maintained in both sexes. These result have been interpreted to have suggested that the hyperactivity of the male X vis-a-vis dosage compensation in Drosophila is primarily a property of the inherent organization of the X chromosome itself and is achieved through modulation in the organization, rather than exclusively through autosomal factor(s), although a secondary level of autosomal regulation has not yet been ruled out.


eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
William S Kruesi ◽  
Leighton J Core ◽  
Colin T Waters ◽  
John T Lis ◽  
Barbara J Meyer

The X-chromosome gene regulatory process called dosage compensation ensures that males (1X) and females (2X) express equal levels of X-chromosome transcripts. The mechanism in Caenorhabditis elegans has been elusive due to improperly annotated transcription start sites (TSSs). Here we define TSSs and the distribution of transcriptionally engaged RNA polymerase II (Pol II) genome-wide in wild-type and dosage-compensation-defective animals to dissect this regulatory mechanism. Our TSS-mapping strategy integrates GRO-seq, which tracks nascent transcription, with a new derivative of this method, called GRO-cap, which recovers nascent RNAs with 5′ caps prior to their removal by co-transcriptional processing. Our analyses reveal that promoter-proximal pausing is rare, unlike in other metazoans, and promoters are unexpectedly far upstream from the 5′ ends of mature mRNAs. We find that C. elegans equalizes X-chromosome expression between the sexes, to a level equivalent to autosomes, by reducing Pol II recruitment to promoters of hermaphrodite X-linked genes using a chromosome-restructuring condensin complex.


2007 ◽  
Vol 27 (24) ◽  
pp. 8760-8769 ◽  
Author(s):  
Kathleen A. Worringer ◽  
Barbara Panning

ABSTRACT In organisms with sex chromosomes, dosage compensation equalizes gene expression between the sexes. In Drosophila melanogaster males, the male-specific lethal (MSL) complex of proteins and two noncoding roX RNAs coat the X chromosome, resulting in a twofold transcriptional upregulation to equalize gene expression with that of females. How MSL complex enrichment on the X chromosome is regulated is not well understood. We performed an RNA interference screen to identify new factors required for dosage compensation. Using a Drosophila Schneider S2 cell line in which green fluorescent protein (GFP)-tagged MSL2 localizes to the X chromosome, we assayed ∼7,200 knockdowns for their effects on GFP-MSL2 distribution. One factor identified is the zinc finger protein Zn72D. In its absence, the MSL complex no longer coats the X chromosome. We demonstrate that Zn72D is required for productive splicing of the transcript for the MSL protein Maleless, explaining the dosage compensation defect. However, Zn72D is required for the viability of both sexes, indicating its functions are not sex specific. Consistent with this, Zn72D colocalizes with elongating RNA polymerase II, implicating it as a more general factor involved in RNA metabolism.


Author(s):  
João D Dias ◽  
Tiago Rito ◽  
Elena Torlai Triglia ◽  
Alexander Kukalev ◽  
Carmelo Ferrai ◽  
...  

2013 ◽  
Author(s):  
Kai Chen ◽  
Jeff Johnston ◽  
Wanqing Shao ◽  
Samuel Meier ◽  
Cynthia Staber ◽  
...  

Author(s):  
Won-Ki Cho ◽  
Namrata Jayanth ◽  
Brian P English ◽  
Takuma Inoue ◽  
J Owen Andrews ◽  
...  

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