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G3 (Bethesda). 2015 Jun 23;5(10):1949-60. doi: 10.1534/g3.115.017921.

Endogenous Small RNA Mediates Meiotic Silencing of a Novel DNA Transposon.

Author information

1
Department of Plant Pathology & Microbiology and Center for Plant Cell Biology, Institute for Integrative Genome Biology, University of California-Riverside, Riverside, California 92521 Plant Sciences Graduate Program, University of California, Riverside, California 92521.
2
Department of Biochemistry and Biophysics, Oregon State University, Corvallis, Oregon 97331.
3
Department of Plant and Microbial Biology, University of California, Berkeley, California 94720.
4
Department of Plant Pathology & Microbiology and Center for Plant Cell Biology, Institute for Integrative Genome Biology, University of California-Riverside, Riverside, California 92521 jason.stajich@ucr.edu.

Abstract

Genome defense likely evolved to curtail the spread of transposable elements and invading viruses. A combination of effective defense mechanisms has been shown to limit colonization of the Neurospora crassa genome by transposable elements. A novel DNA transposon named Sly1-1 was discovered in the genome of the most widely used laboratory "wild-type" strain FGSC 2489 (OR74A). Meiotic silencing by unpaired DNA, also simply called meiotic silencing, prevents the expression of regions of the genome that are unpaired during karyogamy. This mechanism is posttranscriptional and is proposed to involve the production of small RNA, so-called masiRNAs, by proteins homologous to those involved in RNA interference-silencing pathways in animals, fungi, and plants. Here, we demonstrate production of small RNAs when Sly1-1 was unpaired in a cross between two wild-type strains. These small RNAs are dependent on SAD-1, an RNA-dependent RNA polymerase necessary for meiotic silencing. We present the first case of endogenously produced masiRNA from a novel N. crassa DNA transposable element.

KEYWORDS:

Neurospora; genome defense; meiotic silencing; small RNA; transposon

PMID:
26109355
PMCID:
PMC4592977
DOI:
10.1534/g3.115.017921
[Indexed for MEDLINE]
Free PMC Article

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