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Review
. 2012 Apr;22(2):156-63.
doi: 10.1016/j.gde.2011.12.004. Epub 2012 Jan 11.

Different means, same end-heterochromatin formation by RNAi and RNAi-independent RNA processing factors in fission yeast

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Review

Different means, same end-heterochromatin formation by RNAi and RNAi-independent RNA processing factors in fission yeast

Francisca E Reyes-Turcu et al. Curr Opin Genet Dev. 2012 Apr.

Abstract

The assembly of heterochromatin in eukaryotic genomes is critical for diverse chromosomal events including regulation of gene expression, silencing of repetitive DNA elements, proper segregation of chromosomes and maintenance of genomic integrity. Previous studies have shown that noncoding RNAs and the RNA interference (RNAi) machinery promote the assembly of heterochromatin that serves as a multipurpose platform for targeting effectors involved in various chromosomal processes. Recent work has revealed that RNAi-independent mechanisms, involving RNA processing activities that utilize both noncoding and coding RNAs, operate in the assembly of heterochromatin. These findings have established that, in addition to coding for proteins, mRNAs also function as signaling molecules that modify chromatin structure by targeting heterochromatin assembly factors.

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Figures

Figure 1
Figure 1
(A) Heterochromatin nucleation is mediated by RNA-based and DNA sequence-based mechanismsRNA-based mechanisms to establish heterochromatin include both RNAi-dependent and RNAi-independent pathways. DNA-sequence based mechanisms rely on sequence specific DNA binding factors to recruit chromatin-modifying activities. (B) RNA-based heterochromatin nucleation pathways. The RNAi-dependent pathway (left) involves RITS, RDRC and Dicer. Guided by siRNAs, the RITS complex localizes to nascent transcripts where it interacts with Stc1, a scaffold that bridges RITS to Clr4. Clr4 methylates H3K9 to assemble heterochromatin. Repeat transcripts are polyadenylated by Mlo3-associated TRAMP, a factor that meditates processing of RNAs by exosome and the RNAi machinery. The RNAi-independent pathway (right) requires the RNA elimination machinery to assemble facultative heterochromatin at meiotic genes. The RNA binding protein Mmi1, along with factors involved in pre-mRNA 3′-end processing and the RNA elimination machinery, recognize specific meiotic RNAs. Red1, a protein that interacts with the exosome, may form a specialized complex that recruits Clr4 required for the assembly of heterochromatin at specific meiotic genes.
Figure 2
Figure 2. Heterochromatin promotes transcriptional silencing through histone deacetylation and changes in nucleosome occupancy
H3K9me that is initially targeted to nucleation sites by DNA- or RNA-based mechanisms can be spread to surrounding sequences via a process that involves Clr4 binding to methylated H3K9. HP1 proteins (Chp2 and Swi6) bound to H3K9me provide a recruiting platform for loading of the histone deacetylase complexes SHREC and Clr6-complex, and the histone chaperones Asf1-HIRA. Clr6 and SHREC have overlapping functions in limiting RNAPII occupancy at heterochrochromatic loci [9]. Asf1-HIRA facilitates deacetylation of histones by Clr6 HDAC. Asf1-HIRA and SHREC also promote nucleosome occupancy and eliminate nucleosome-free regions (NFRs) that are thought to prevent access to the transcriptional machinery and enforce transcriptional gene silencing.

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References

    1. Grewal SI, Jia S. Heterochromatin revisited. Nat Rev Genet. 2007;8:35–46. - PubMed
    1. Trojer P, Reinberg D. Facultative heterochromatin: is there a distinctive molecular signature? Mol Cell. 2007;28:1–13. - PubMed
    1. Jenuwein T, Allis CD. Translating the histone code. Science. 2001;293:1074–1080. - PubMed
    1. Bannister AJ, Zegerman P, Partridge JF, Miska EA, Thomas JO, Allshire RC, Kouzarides T. Selective recognition of methylated lysine 9 on histone H3 by the HP1 chromo domain. Nature. 2001;410:120–124. - PubMed
    1. Nakayama J, Rice JC, Strahl BD, Allis CD, Grewal SI. Role of histone H3 lysine 9 methylation in epigenetic control of heterochromatin assembly. Science. 2001;292:110–113. - PubMed

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