RID is required for both repeat-induced point mutation and nucleation of a novel transitional heterochromatic state for euchromatic repeats

To maintain genome integrity, repeat sequences are subject to heterochromatin inactivation and, in Neurospora, repeat-induced point mutation (RIP). The initiating factors behind both are poorly understood. We resolve the paradoxical observation that newly introduced Repeat-Linker-Repeat (R-L-R) constructs require RID alone for RIP, while genomic repeats are RIPed in the absence of RID, showing that eu- and hetero- chromatic repeats are handled differently, the latter additionally requiring DIM-2. The differences between mechanisms associated with older and newer duplicates caution against extrapolation from mechanisms inferred from model experimental systems. Additionally, while chromatin status affects RIP, we also show that RID, when tethered with LexA, acts as a nucleation center for the transition from euchromatin to heterochromatin in an HDA-1 dependent fashion. Constitutive heterochromatin by contrast is largely HDA1 independent and depends on HDA-1 paralogs. RID is thus a dual function initiator of both RIP and the transition to heterochromatin.

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Publication Details

Journal
Nucleic Acids Research
Published
2025-03-20
DOI
https://doi.org/10.1093/nar/gkaf263
Citations
4
Primary Topic
Fungal and yeast genetics research
Type
article
Field-Weighted Citation Impact
3.22

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article

RID is required for both repeat-induced point mutation and nucleation of a novel transitional heterochromatic state for euchromatic repeats

Ruonan Yao, Huawei Tan, Laurence D. Hurst, Xiaonan Chen et al.
4 citations
Nucleic Acids Research
Fungal and yeast genetics research
3.22
article

RID is required for both repeat-induced point mutation and nucleation of a novel transitional heterochromatic state for euchromatic repeats

Ruonan Yao, Huawei Tan, Laurence D. Hurst, Xiaonan Chen, Nannan Wu, Jingxuan Chen, Sihai Yang, Ju Huang, Zhen He, Long Wang, Lan Xue, Yingying Sun
article en
4 citations

Abstract

To maintain genome integrity, repeat sequences are subject to heterochromatin inactivation and, in Neurospora, repeat-induced point mutation (RIP). The initiating factors behind both are poorly understood. We resolve the paradoxical observation that newly introduced Repeat-Linker-Repeat (R-L-R) constructs require RID alone for RIP, while genomic repeats are RIPed in the absence of RID, showing that eu- and hetero- chromatic repeats are handled differently, the latter additionally requiring DIM-2. The differences between mechanisms associated with older and newer duplicates caution against extrapolation from mechanisms inferred from model experimental systems. Additionally, while chromatin status affects RIP, we also show that RID, when tethered with LexA, acts as a nucleation center for the transition from euchromatin to heterochromatin in an HDA-1 dependent fashion. Constitutive heterochromatin by contrast is largely HDA1 independent and depends on HDA-1 paralogs. RID is thus a dual function initiator of both RIP and the transition to heterochromatin.

Nucleic Acids ResearchVol. 53(6)
Nanjing Agricultural University (CN), Nanjing Forestry University (CN), Pharmaceutical Biotechnology (Czechia) (CZ), University of Bath (GB), Nanjing University (CN)
Joint Information Systems Committee, National Natural Science Foundation of China, China Agricultural University, Chinese Academy of Sciences, Government of Jiangsu Province, Natural Science Foundation of Jiangsu Province, Jiangsu Collaborative Innovation Center for Modern Crop Production, Directorate for Biological Sciences, National Key Research and Development Program of China, Fundamental Research Funds for the Central Universities, Natural Science Foundation of Jiangsu Province for Distinguished Young Scholars
Openalex Percentile: Top 9%
Fungal and yeast genetics research
3.22
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