ArticlePLoS genetics2012
Maize Unstable factor for orange1 is required for maintaining silencing associated with paramutation at the pericarp color1 and booster1 loci.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- RNA-directed DNA methylation mutants reduce histone methylation at the paramutated maize booster1 enhancer.Plant physiology · 2024Article
- Paramutation at the maize pl1 locus is associated with RdDM activity at distal tandem repeats.PLoS genetics · 2024Article
- Article
- CHROMOMETHYLTRANSFERASE3/KRYPTONITE maintains theProceedings of the National Academy of Sciences of the United States of America · 2022Article
- The Dominant and Poorly Penetrant Phenotypes of MaizeThe Plant cell · 2018Article
- Article
- Paramutation and related phenomena in diverse species.Nature reviews. Genetics · 2017Review
- P1 Epigenetic Regulation in Leaves of High Altitude Maize Landraces: Effect of UV-B Radiation.Frontiers in plant science · 2016Article
- Trans-Homolog Interactions Facilitating Paramutation in Maize.Plant physiology · 2015Review
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5 authors at 2 institutions in 1 country.
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Abstract
To understand the molecular mechanisms underlying paramutation, we examined the role of Unstable factor for orange1 (Ufo1) in maintaining paramutation at the maize pericarp color1 (p1) and booster1 (b1) loci. Genetic tests revealed that the Ufo1-1 mutation disrupted silencing associated with paramutation at both p1 and b1. The level of up regulation achieved at b1 was lower than that at p1, suggesting differences in the role Ufo1-1 plays at these loci. We characterized the interaction of Ufo1-1 with two silenced p1 epialleles, P1-rr' and P1-pr(TP), that were derived from a common P1-rr ancestor. Both alleles are phenotypically indistinguishable, but differ in their paramutagenic activity; P1-rr' is paramutagenic to P1-rr, while P1-pr(TP) is non-paramutagenic. Analysis of cytosine methylation revealed striking differences within an enhancer fragment that is required for paramutation; P1-rr' exhibited increased methylation at symmetric (CG and CHG) and asymmetric (CHH) sites, while P1-pr(TP) was methylated only at symmetric sites. Both silenced alleles had higher levels of dimethylation of lysine 9 on histone 3 (H3K9me2), an epigenetic mark of silent chromatin, in the enhancer region. Both epialleles were reactivated in the Ufo1-1 background; however, reactivation of P1-rr' was associated with dramatic loss of symmetric and asymmetric cytosine methylation in the enhancer, while methylation of up-regulated P1-pr(TP) was not affected. Interestingly, Ufo1-1-mediated reactivation of both alleles was accompanied with loss of H3K9me2 mark from the enhancer region. Therefore, while earlier studies have shown correlation between H3K9me2 and DNA methylation, our study shows that these two epigenetic marks are uncoupled in the Ufo1-1-reactivated p1 alleles. Furthermore, while CHH methylation at the enhancer region appears to be the major distinguishing mark between paramutagenic and non-paramutagenic p1 alleles, H3K9me2 mark appears to be important for maintaining epigenetic silencing.
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