Skip Navigation

Nucleic Acids Research 2004 32(14):4237-4243; doi:10.1093/nar/gkh764
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (334K) Freely available
Right arrow Supplementary Material
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (18)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Chicas, A.
Right arrow Articles by Macino, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Chicas, A.
Right arrow Articles by Macino, G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published online 9 August 2004

Nucleic Acids Research, Vol. 32 No. 14 © Oxford University Press 2004; all rights reserved

RNAi-dependent and RNAi-independent mechanisms contribute to the silencing of RIPed sequences in Neurospora crassa

Agustin Chicas, Carlo Cogoni and Giuseppe Macino*

Istituto Pasteur e Fondazione Cenci Bolognetti, Dipartimento di Biotecnologie Cellulari ed Ematologia, Sezione di Genetica Molecolare, Università di Roma ‘La Sapienza’, Viale Regina Elena, 324, 00161 Roma, Italy

* To whom correspondence should be addressed. Tel: +39 064457731; Fax: +39 064457731; Email: macino{at}bce.uniroma1.it

Received June 16, 2004; Revised and Accepted July 26, 2004

RNA interference (RNAi) can silence genes at the transcriptional level by targeting locus-specific Lys9H3 methylation or at the post-transcriptional level by targeting mRNA degradation. Here we have cloned and sequenced genomic regions methylated in Lys9H3 in Neurospora crassa to test the requirements for components of the RNAi pathway in this modification. We find that 90% of clones map to repeated sequences and relics of transposons that have undergone repeat-induced point mutations (RIP). We find siRNAs derived from transposon relics indicating that the RNAi machinery targets these regions. This is confirmed by the fact that the presence of these siRNAs depends on components of the RNAi pathway such as the RdRP (QDE-1), the putative RecQ helicase (QDE-3) and the two Dicer enzymes. We show that Lys9H3 methylation of RIP sequences is not affected in mutants of the RNAi pathway indicating that the RNAi machinery is not involved in transcriptional gene silencing in Neurospora. We find that RIP regions are transcribed and that the transcript level increases in the mutants of the RNAi pathway. These data suggest that the biological function of the Neurospora RNAi machinery is to control transposon relics and repeated sequences by targeting degradation of transcripts derived from these regions.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 GeneticsHome page
J. A. Casas-Mollano, J. Rohr, E.-J. Kim, E. Balassa, K. van Dijk, and H. Cerutti
Diversification of the Core RNA Interference Machinery in Chlamydomonas reinhardtii and the Role of DCL1 in Transposon Silencing
Genetics, May 1, 2008; 179(1): 69 - 81.
[Abstract] [Full Text] [PDF]

Home page
 Eukaryot CellHome page
T. M. Hammond, J. W. Bok, M. D. Andrewski, Y. Reyes-Dominguez, C. Scazzocchio, and N. P. Keller
RNA Silencing Gene Truncation in the Filamentous Fungus Aspergillus nidulans
Eukaryot. Cell, February 1, 2008; 7(2): 339 - 349.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
F. Wang, N. Koyama, H. Nishida, T. Haraguchi, W. Reith, and T. Tsukamoto
The assembly and maintenance of heterochromatin initiated by transgene repeats are independent of the RNA interference pathway in Mammalian cells.
Mol. Cell. Biol., June 1, 2006; 26(11): 4028 - 4040.
[Abstract] [Full Text] [PDF]

Home page
 Eukaryot CellHome page
M. A. Walti, C. Villalba, R. M. Buser, A. Grunler, M. Aebi, and M. Kunzler
Targeted Gene Silencing in the Model Mushroom Coprinopsis cinerea (Coprinus cinereus) by Expression of Homologous Hairpin RNAs.
Eukaryot. Cell, April 1, 2006; 5(4): 732 - 744.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
S. R. Lee and K. Collins
Two classes of endogenous small RNAs in Tetrahymena thermophila
Genes & Dev., January 1, 2006; 20(1): 28 - 33.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
M. Yoshikawa, A. Peragine, M. Y. Park, and R. S. Poethig
A pathway for the biogenesis of trans-acting siRNAs in Arabidopsis
Genes & Dev., September 15, 2005; 19(18): 2164 - 2175.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
E. P. Murchison, J. F. Partridge, O. H. Tam, S. Cheloufi, and G. J. Hannon
Characterization of Dicer-deficient murine embryonic stem cells
PNAS, August 23, 2005; 102(34): 12135 - 12140.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
T. Nolan, L. Braccini, G. Azzalin, A. De Toni, G. Macino, and C. Cogoni
The post-transcriptional gene silencing machinery functions independently of DNA methylation to repress a LINE1-like retrotransposon in Neurospora crassa
Nucleic Acids Res., March 14, 2005; 33(5): 1564 - 1573.
[Abstract] [Full Text] [PDF]

Home page
 GeneticsHome page
T. M. Hammond and N. P. Keller
RNA Silencing in Aspergillus nidulans Is Independent of RNA-Dependent RNA Polymerases
Genetics, February 1, 2005; 169(2): 607 - 617.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.