The long non‐coding RNALINDA restrains cellular collapse following DNA damage in Arabidopsis thaliana

Author:

Herbst Josephine123ORCID,Nagy Solveig Henriette1,Vercauteren Ilse23ORCID,De Veylder Lieven23ORCID,Kunze Reinhard1ORCID

Affiliation:

1. Department of Biology, Chemistry and Pharmacy, Molecular Genetics of Plants, Institute of Biology Freie Universität Berlin Berlin D‐14195 Germany

2. Department of Plant Biotechnology and Bioinformatics Ghent University Ghent B‐9052 Belgium

3. Center for Plant Systems Biology VIB Ghent B‐9052 Belgium

Abstract

SUMMARYThe genomic integrity of every organism is endangered by various intrinsic and extrinsic stresses. To maintain genomic integrity, a sophisticated DNA damage response (DDR) network is activated rapidly after DNA damage. Notably, the fundamental DDR mechanisms are conserved in eukaryotes. However, knowledge about many regulatory aspects of the plant DDR is still limited. Important, yet little understood, regulatory factors of the DDR are the long non‐coding RNAs (lncRNAs). In humans, 13 lncRNAs functioning in DDR have been characterized to date, whereas no such lncRNAs have been characterized in plants yet. By meta‐analysis, we identified the putative long intergenic non‐coding RNA induced by DNA damage (LINDA) that responds strongly to various DNA double‐strand break‐inducing treatments, but not to replication stress induced by mitomycin C. After DNA damage, LINDA is rapidly induced in an ATM‐ and SOG1‐dependent manner. Intriguingly, the transcriptional response of LINDA to DNA damage is similar to that of its flanking hypothetical protein‐encoding gene. Phylogenetic analysis of putative Brassicales and Malvales LINDA homologs indicates that LINDA lncRNAs originate from duplication of a flanking small protein‐encoding gene followed by pseudogenization. We demonstrate that LINDA is not only needed for the regulation of this flanking gene but also fine‐tuning of the DDR after the occurrence of DNA double‐strand breaks. Moreover, Δlinda mutant root stem cells are unable to recover from DNA damage, most likely due to hyper‐induced cell death.

Funder

Deutsche Forschungsgemeinschaft

Publisher

Wiley

Subject

Cell Biology,Plant Science,Genetics

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