ArticlePLoS genetics2021
Histone demethylase AMX-1 is necessary for proper sensitivity to interstrand crosslink DNA damage.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- PARP-2 catalytic activity drives replication-ICL repair in an allele-specific manner during germline development.PLoS genetics · 2026Article
- Paclitaxel-induced germline DNA-damage signatures independent of mismatch repair inFrontiers in pharmacology · 2026Article
- Herbal Extract-Induced DNA Damage, Apoptosis, and Antioxidant Effects ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Therapeutic Potential ofPharmaceuticals (Basel, Switzerland) · 2025Article
- LSD2 Is an Epigenetic Player in Multiple Types of Cancer and Beyond.Biomolecules · 2024Review
- Exploring the Impact ofNutrients · 2023Article
- Histone post-translational modification and the DNA damage response.Genes & diseases · 2023Review
- Histone Demethylase AMX-1 Regulates Fertility in a p53/CEP-1 Dependent Manner.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Histone methylation is dynamically regulated to shape the epigenome and adjust central nuclear processes including transcription, cell cycle control and DNA repair. Lysine-specific histone demethylase 2 (LSD2) has been implicated in multiple types of human cancers. However, its functions remain poorly understood. This study investigated the histone demethylase LSD2 homolog AMX-1 in C. elegans and uncovered a potential link between H3K4me2 modulation and DNA interstrand crosslink (ICL) repair. AMX-1 is a histone demethylase and mainly localizes to embryonic cells, the mitotic gut and sheath cells. Lack of AMX-1 expression resulted in embryonic lethality, a decreased brood size and disorganized premeiotic tip germline nuclei. Expression of AMX-1 and of the histone H3K4 demethylase SPR-5 is reciprocally up-regulated upon lack of each other and the mutants show increased H3K4me2 levels in the germline, indicating that AMX-1 and SPR-5 regulate H3K4me2 demethylation. Loss of AMX-1 function activates the CHK-1 kinase acting downstream of ATR and leads to the accumulation of RAD-51 foci and increased DNA damage-dependent apoptosis in the germline. AMX-1 is required for the proper expression of mismatch repair component MutL/MLH-1 and sensitivity against ICLs. Interestingly, formation of ICLs lead to ubiquitination-dependent subcellular relocalization of AMX-1. Taken together, our data suggest that AMX-1 functions in ICL repair in the germline.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.