Most microRNAs in the single-cell alga Chlamydomonas reinhardtii are produced by Dicer like 3-mediated cleavage of introns and untranslated regions of coding RNAs
Valli, Adrian A
Santos, Bruno ACM
Bassett, Andrew R
Cold Spring Harbor Laboratory Press
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Valli, A. A., Santos, B. A., Hnatova, S., Bassett, A. R., Molnar, A., Chung, B., & Baulcombe, D. (2016). Most microRNAs in the single-cell alga Chlamydomonas reinhardtii are produced by Dicer like 3-mediated cleavage of introns and untranslated regions of coding RNAs. Genome Research, 26 519-519. https://doi.org/10.1101/gr.199703.115
We describe here a forward genetic screen to investigate the biogenesis, mode of action and biological function of miRNA-mediated RNA silencing in the model algal species Chlamydomonas reinhardtii. Amongst the mutants from this screen there were three at Dicer-like 3 that failed to produce both miRNAs and siRNAs and others affecting diverse post-biogenesis stages of miRNA-mediated silencing. The DCL3-dependent siRNAs fell in to several classes including transposon- and repeat-derived siRNAs as in higher plants. The DCL3-dependent miRNAs differ from those of higher plants, however, in that many of them are derived from mRNAs or from the introns of pre-mRNAs. Transcriptome analysis of the wild type and dcl3 mutant strains revealed a further difference from higher plants in that the sRNAs are rarely negative switches of mRNA accumulation. The few transcripts that were more abundant in dcl3 mutant strains than in wild type cells were not due to sRNA-targeted RNA degradation but to direct DCL3 cleavage of miRNA and siRNA precursor structures embedded in the untranslated (and translated) regions of the mRNAs. Our analysis reveals that the miRNA-mediated RNA silencing in C. reinhardtii differs from that of higher plants, and informs about the evolution and function of this pathway in eukaryotes.
algae, RNA silencing, microRNAs, Dicer
Work in the Baulcombe laboratory is supported by the Balzan Prize award and the ERC Advanced Investigator Grant ERC-2013-AdG 340642 TRIBE. AAV was supported by a Marie-Curie fellowship (PIEF-GA-2010-276037). BYC was supported by an EMBL long-term postdoctoral fellowship and a Sir Henry Wellcome Fellowship (096082). DCB is the Royal Society Edward Penley Abraham Research Professor.
Wellcome Trust (096082/Z/11/Z)
European Research Council (340642)
External DOI: https://doi.org/10.1101/gr.199703.115
This record's URL: https://www.repository.cam.ac.uk/handle/1810/253852
Licence URL: http://creativecommons.org/licenses/by/4.0/